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CLINICAL 
■  AeCTROC  ARDIOGRAPHY. 


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CLINICAL 
ELECTROCARDIOGRAPHY 


BY 


THOMAS  LEWIS,  M.D.,  F.R.S.,  D.Sc,  F.R.C.P. 

Physician  of  the  Staff  of  the  Medical  Research  Committee;  Assistant  Physician 

and  Lecturer  on  Cardiac  Pathology,   University  College  Hospital; 

Late  Physician  to  Out-Patients,  City  of  London  Hospital 


i§>econiJ  €bttton 


NEW  YORK 

PAUL  B.  HOEBER 
1919 


By  the  same  Author: 
Clinical  Disorders  of  the  Heart  Beat 

Fifth  Edition  in  Press 

Clinical  Electrocardiography 

Second  Edition,  $2.50  net 

The  Soldier's  Heart  and  the  Effort 
Syndrome  $2.50  net 

Lectures  on  the  Heart  $2.50  net 

The  Mechanism  and  Graphic 
Registration  of  the  Heart  Beat 

With  Especial  Reference  to  its  Clinical  Pathology 

$16.00  net 

Heart 

A  Journal  for  the  Study  of  the  Circulation 
Edited  by  Thomas  Lewis.    Per  volume,  $7.00  net 


PAUL  B.  HOEBER,  Publisher 
67'6o  East  59TH  Street,  New  York 


1= 


PREFACE. 

TN  republishing  an  account  of  clinical  electro- 
cardiography, I  do  so  from  conviction  that  this 
method  of  examination  is  essential  to  the  modern 
diagnosis  and  treatment  of  cardiac  patients.  When 
some  nine  years  ago  I  commenced  to  study  disorders 
of  the  heart  with  the  aid  of  the  "  string  galvanometer  " 
the  method  was  in  its  early  infancy  ;  although  it  was 
regarded  at  that  time  as  full  of  promise,  yet  its  scope, 
in  helping  to  perfect  our  acquaintanceship  with  heart 
disease,  could  not  then  be  foreseen.  Electrocardio- 
graphy has  taken  us  far,  having  filled  great  gaps  in  our 
knowledge  of  these  maladies  ;  for  it  is  a  means  of 
directly  examining  the  all-essential  heart  muscle. 

Those  cardiac  patients  are  few  in  whom  an 
electric  examination  is  superfluous,  and  in  a  large 
percentage   of   cases   the   records    profoundly   modify 


iv.  Preface. 

our  conceptions  of  the  malady  which  we  treat.  The 
time  has  come  when  no  hospital  which  undertakes 
the  care  of  many  of  these  patients  may  neglect  the 
string  galvanometer,  if  it  is  to  rank  amongst  institutions 
whose  design  is  proficiency. 

Electrocardiography  has  developed  ;  it  has  grown 
along  technical  lines  ;  it  has  embraced  a  terminology 
of  its  own,  the  inevitable  result  of  progress  in  a  new 
direction.  It  has  done  its  share  in  increasing  the 
already  overweighted  burden  of  general  medicine. 
We  may  not  deplore,  but  should  welcome  the  fullness 
of  this  load ;  recognising  in  it  an  increase  of  our 
capacity. 

In  Clinical  Disorders  of  the  Heart  Beat  I  have 
attempted  to  collect  the  simple  bedside  signs  of 
disordered  heart  action  and  to  narrate  their  influence 
upon  prognosis  and  treatment  in  a  manner  palatable 
to  pure  clinicians.  The  present  chapters  supplement 
that  book.  They  are  intended  to  serve  as  an 
introduction  to  students  of  electrocardiography  and 
especially    as    a   guide   to    practitioners    and   hospital 


Preface.  v. 

physicians  in  understanding  curves  which  may  be 
taken  by  others  from  patients  in  their  charge.  Thej^ 
describe  in  outline  the  most  precise  method  which  we 
possess,  when  we  attempt  to  identify  the  many  forms 
of  disordered  heart  action.  It  frequently  happens 
that  other  graphic  methods  fail  to  analyse  these 
disturbances  ;  electrocardiography  is  the  last  court 
of  appeal  and  its  judgment  is  almost  infallible.  There 
are  types  of  heart  action  upon  which  other  methods 
are  almost,  if  not  quite,  silent ;  knowledge  of  these 
conditions  is  in  the  almost  exclusive  possession  of 
electrocardiography.  Finally,  the  electric  curves  have 
revealed  a  number  of  new  signs,  associated  with 
abnormal  distribution  of  the  muscular  masses  in  the 
heart,  or  with  abnormalities  in  the  course  taken  by 
that  excitation  wave  which  immediately  precedes 
and  traces  out  the  path  of  the  contraction  wave. 

In  writing  of  Clinical  Electrocardiography  I  confine 
myself  to  common  varieties  of  disorder  and  to  electric 
signs  which  are  frequently  to  be  observed.  I  do  not 
submit    the    evidences    for    mv    conclusions    in    this 


vi.  Preface. 

handbook,  seeing  that  these  evidences  are  fully  set 
forth  in  my  larger  treatise,  The  Mechanism  and 
Graphic  Registration  of  the  Heart  Beat,  now  in  course 
of  preparation. 

I  am  greatly  obliged  to  Dr.  H.  J.  Starling  for 
his  careful  revision  of  the  proof  sheets. 

T.  L. 

September,  1917. 


CONTENTS. 


CHAPTER  I. 

The  Electrocardiographic  Method 

Connection  of  patient 

The  compensatory  circuit 

The  standardiser 
The  method  of  obtaining  standardised  electrocardiograms 
Checking  the  accuracy  of  standardised  curves 
Testing  certain  properties  of  the  string.  . 

CHAPTER  II. 

The  Physiological  Electrocardiogram 

The  physiological  auricular  complex 
The  physiological  ventricular  complex 


Page. 

1 
5 

7 
7 
7 
9 
11 


13 
17 

17 


CHAPTER  III. 

Rhythmic  but  Anomalous  Electrocardiograms 
The  constitution  of  the  ventricular  complex 
Aberrant  beats        .  . 

Preponderance  of  left  or  right  ventricle.  . 
Inversion  of  "  T  " 


23 
24 
27 
30 
35 


CHAPTER  IV. 


Auriculo -Ventricular  Heart-Block 
Partial  heart-block 
Complete  heart-block 
Slow  action  of  the  ventricle 


36 
36 
43 
47 


V11I. 


Contents. 


CHAPTER  V. 

Premature  Contractions  or  Extrasystoles             .  .          .  .  .  .  52 

Premature  contractions  of  ventricular  origin    .  .           .  .  .  .  52 

Premature  contractions  of  auricular  origin       .  .           .  .  .  .  59 

Premature  contractions  arising  in  the  functional  tissues  .  .  65 


CHAPTER  VI. 

Simple  Paroxysmal  Tachycardia 

Dislocation  of  the  pacemaker 


66 
73 


CHAPTER  VII. 


Auricular  Flutter 

The  electrocardiograms 


75 

76 


CHAPTER  VIII. 


Auricular  Fibrillation  .  . 


85 


CHAPTER  IX. 

Sinus  Disturbances  and  Alternation 

Respiratory  arrhythmia  and  allied  irregularities 
Sino -auricular  heart-block 
Alternation  of  the  heart 


96 
96 
98 
98 


CHAPTER  X. 

Special  Conditions 

Electrocardiograms  in  valve  lesions,  etc. 
Mitral  stenosis 
Aortic  disease 
Mitral  regurgitation 
Congenital  heart  affections  .  . 
Renal  diseases  and  high  blood-pressure 
Exophthalmic  goitre 


101 
101 
103 
J06 
108 
108 
111 
112 


Chapter   I. 


THE    ELECTROCARDIOGRAPHIC    METHOD. 

That  electric  currents  are  developed  in  the  heart  at  each 
contraction  of  this  organ  was  demonstrated  in  the  middle  of 
the  nineteenth  century.  Modern  electrocardiography  is 
the  outcome  of  this  discovery.  The  currents  are  small,  yet 
modern  instruments  are  sufficiently  sensitive  to  record  them 
with  facility.  It  is  even  unnecessary  that  the  heart  should 
be  exposed  ;  the  currents  will  deflect  a  suitable  galvanometer 
when  the  latter  is  connected  to  the  limbs  of  the  human  subject, 
as  Waller  first  showed.  It  is  the  study  of  the  direction,  time 
relations  and  magnitude  of  these  currents  which  constitutes 
modern  electrocardiography. 

The  instrument  which  is  described  in  the  present  chapter 
is  know  as  the  "  string  galvanometer,"  the  invention  of 
Einthoven,  a  Dutch  physiologist.  It  consists  essentially 
of  a  powerful  electro-magnet,  the  poles  of  which  are  closely 
approximated  (Fig.  1)  ;  and  of  an  extremely  delicate  con- 
ducting fibre  of  silvered  quartz  or  glass  which  is  stretched 
in  the  narrow  gap  between  the  two  magnetic  poles.  If 
minute  currents  are  led  through  this  fibre,  as  it  lies  in  the 
magnetic  field,  the  fibre  moves  across  the  gap  in  response 
to  the  tested  current  in  a  plane  at  right  angles  to  the  lines 
of    magnetic    force.        The    magnified    shadow    of    the    fibre 


2  Chapter  I. 

is  vertical  and  is  projected  by  means  of  an  optical  system 
and  powerful  light  on  to  the  horizontal  slit  of  a  camera  ; 
the  shadow  moves  at  right  angles  to  and  across  the  slit  and 
the  movements  are  photographed  upon  a  sensitive  plate 
which  travels  behind  the  slit.  I  do  not  propose  to  describe 
the  detailed  construction   of  the   galvanometer  itself  or  of 


Fig.  1.  A  diagram  illustrating  the  construction  of  the  string  galvanometer. 
The  poles  of  the  magnet  ( N ,  S)  are  seen  in  outline ;  the  recording  fibre 
iCC)  lies  vertically  between  them  ;  its  movements  may  be  observed 
through  a  microscope  (Z>).  The  movements  of  the  string  are  in  a  plane 
parallel  to  the  faces  of  the  magnetic  poles,  as  indicated  by  the  central 
arrow.     J7  is  a  condenser. 


the  accessory  apparatus  which  it  is  necessary  to  employ  in 
obtaining  human  electrocardiograms.  Many  different 
installations  are  now  sold  and  some  are  specially  arranged  for 
clinical  purposes.  The  galvanometer  illustrated  in  Fig.  2 
is  perhaps  the  most  serviceable  of  any,  and  is  to  be  recom- 
mended for  the  simplicity  of  its  construction  and  the  ease 
with   which   it   is   kept   in    order    and    manipulated.       The 


The   Electrocardiographic  Method. 
N 


Fig.  2.  The  string  galvanometer,  as  modelled  by  the  Cambridge  Scientific 
Instrument  Company.  The  coils  of  the  magnet  (B,  B)  are  seen  in  the 
background ;  they  are  supplied  with  current  through  the  four  terminals 
(M,  N)  ;  the  poles  of  the  magnet  (A)  are  in  the  foreground.  The  magnet  is 
pierced  by  microscope  (6)  and  condenser  (  D,  D).  The  string  is  encased 
in  a  carrier  (E),  which  is  suspended  from  above  upon  two  knife  edge 
rests  ( K,  K)  and  hangs  between  the  magnetic  poles.  The  string 
tension  is  adjusted  by  means  of  the  milled  screw  ( J) ;  the  position  of  the 
carrier  in  the  field  is  altered  by  an  adjustment  at  F.  The  tested  current 
is  led  to  the  instrument  through  the  two  terminals  0  and  P. 


adjustments  are  simple  and  consist  of  mill-headed  screws 
which  level  the  instrument,  centre  the  fibre  in  the  field, 
increase  or  decrease  its  tension,  and  focus  its  shadow  upon 
the  camera.  Those  who  desire  a  more  detailed  account  of 
the  apparatus  may  refer  to  the  special  descriptions  issued 

B  2 


4  Chapter   I. 

by  its  makers,  or  to  my  book,  The  Mechanism  and  Graphic 
Registration  of  the  Heart  Beat  ;  but  familiarity  with  galvano- 
metric  outfits  can  be  gained  only  by  intimate  acquaintanceship 
with  working  instruments. 

The  galvanometer  is  connected  to  the  patient  through 
some  special  form  of  switchboard,  Students  of  electro- 
cardiography utilise  switchboards  of  different  patterns,  more 


/o  camera 
-  -<- —  -  - 


from  /an/ern 


R.A 


S  ha nde rdiser 


Fig.  3.     A  switchboard  arranged  as  a  group  of  simple  circuits  and  connected 
to  the  galvanometer. 


or  less  complicated  ;  those  supplied  for  clinical  use  are 
arranged  to  insure  speedy  and  accurate  work  ;  the  actual 
switches  are  therefore  few  in  number  but  the  wiring  is  intricate. 
I  propose  to  describe  a  scheme  which  may  be  drawn  as  a 
group  of  simple  circuits.  This  scheme,  though  serviceable, 
is  no  longer  in  clinical  use,  because  the  number  of  the  keys. 


The   Electrocardiographic  Method.  5 

makes  the  manipulation  of  the  board  relatively  slow.  But 
I  retain  it  as  an  illustration  because  its  circuits  and  their  use 
are  easy  to  understand  and  because  more  complex  boards 
are  arranged  on  similar  principles. 

Fig.  3  is  a  diagram  of  the  apparatus  and  its  connections. 
The  string  of  the  galvanometer  (G8)  is  connected  to  a  key 
( K1)  which  closes  the  string  circuit.  The  closure  of  this  key 
brings  the  string  to  rest  and  safeguards  it  from  damage. 
The  same  key  communicates  with  two  circuits,  the  inner 
and  outer  circles  of  the  diagram  ;  the  former  is  a  shunt, 
containing  a  resistance  and  key  ( R1  and  K2),  so  arranged  that 
when  closed  it  carries  the  greater  part  of  the  tested  current, 
thus  preserving  the  string  from  mishap.  It  is  used  when 
a  current  of  unknown  strength  is  thrown  into  the  string 
circuit.  The  outer  circle  represents  the  main  circuit  ;  it 
is  broken  at  three  points  ;  (1)  at  K1  where  it  joins  the  string 
circuit,  (2)  at  C1,  by  a  commutator,  where  it  connects  to  the 
patient,  and  (3)  at  C2,  by  a  commutator,  where  it  connects 
to  the  compensator.  It  contains  also  a  dial  resistance  (R5) 
and  the  standardiser.  The  separate  parts  of  the  apparatus 
may  be  described  briefly  and  in  rotation. 

Connection  of  patient.  One  wire  which  runs  from  the 
commutator  C1  to  the  key  K5  may  be  connected  at  will  to 
the  right  arm  (R.  A.)  or  left  arm  (L.  A.)  by  means  of  the 
special  key  ;  the  second  or  parallel  wire  may  be  connected 
to  the  left  arm  or  left  leg  (L.  L.)  by  the  same  key.*  The 
actual  contacts  are  made  when  the  limbs  are  immersed  in 
salt  water,  f  and  through  porous  pots  containing  zinc  sulphate 
(Fig.  3  B  and  Fig.  4).  The  key  (K5)  is  arranged  so  that  the 
two  main  wires  may  have  the  following  paired  connections. 

*  The  wires  which  connect  to  the  limbs  may  be  of  any  length  ;  the 
patient  who  is  observed  may  be  in  a  separate  building. 

f  The  water  should  be  warm  and  pieces  of  cotton  wool  may  be  added  to 
form  a  bath  of  porridgedike  consistency.  By  these  means  movements  of 
hands   and   tremor   are   diminished. 


Chapter  I. 


Fig.  4.  Photograph  of  a  subject  as  connected  for  observation.  The  two 
arms  and  the  left  leg  are  used,  and  curves  are  taken  from  the  three  leads 
which  are  represented  by  arrows  in  the  figure.  The  zinc  sulphate  is 
placed  in  the  outer  vessels  of  the  electrodes  shown  in  this  figure. 


Limbs  connected. 

Lead  I       .  .  ..  .  .      R.  A.  and   L.  A. 

Lead   II     ..  .  .  ..      R.  A.  and   L.   L. 

Lead  III  . .  .  .  .  .      L.   A.  and  L.   L. 

These   are  the  connections  which  are   employed  in  routine 
observation. 


The  Electrocardiographic  Method.  7 

The  compensatory  circuit.  This  is  shown  to  the  right  in 
Fig.  3  ;  and  consists  of  an  accumulator  (A),  key  ( K3),  suitable 
resistance  (R2  —  19  ohms)  and  slide  wire  (W  W  =  1  ohm). 
It  is  used  to  bring  the  string  shadow  to  zero  when  the  patient  is 
connected  to  the  galvanometer  ;  it  serves  to  neutralise  the 
current  derived  from  the  skin,  generally  referred  to  as  the 
"  skin  current,"  and  is  fitted  with  a  commutator,  C2,  which 
reverses  the  direction  of  the  compensatory  current. 

The  standardiser  is  formed  by  a  similar  circuit  to  that 
of  the  compensator,  consisting  of  a  battery,  suitable  resistances 
(R*  and  R*)  and  key  (i£4).  It  throws  an  E.  M.  F.  of  3 
millivolts  into  the  main  circuit,  and  is  used  to  standardise 
the  string  excursion,  so  that  all  electrocardiograms  may  be 
comparable  one  with  another. 

The  dial  resistance  R5  serves  many  purposes  ;  amongst 
others,  the  measurement  of  the  resistance  of  the  string  or 
of  the  patient's  body. 

The  method  of  obtaining  standardised  electrocardiograms. 

Standardised  electrocardiograms  are  obtained  in  the 
following  manner. 

1.  With  the  compensatory  and  standardising  circuits 
open,  but  with  the  shunt  (K2)  closed  and  the  patient  in 
circuit  (K5  connecting  to  R.  A.  and  L.  A.,  the  first  lead),  K1 
is  opened.  The  string  shadow  immediately  takes  up  a  new 
position,  as  a  result  of  skin  current  flowing  into  the  galvano- 
meter, and  shows  minute  electrocardiograms  (Fig.  5a). 

2.  K3  is  closed  and  a  compensatory  current,  or  current 
to  balance  the  skin  current,  is  introduced  which  brings  the 
string  shadow  to  zero  once  again  (Fig.  56). 


Chapter   I. 


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The   Electrocardiographic  Method.  9 

3.  The  shunt  (  K2)  is  opened  and  the  string  moves  again* 
showing  larger  electrocardiograms  (Fig.  5c),  because  the  whole 
current  is  now  allowed  to  flow  through  the  string. 

4.  If  the  string  shadow  has  moved  much  to  one  side, 
it  is  again  brought  to  zero  by  moving  the  slider  of  the 
compensator. 

5.  The  standardising  circuit  (3  millivolts)  is  now  made 
and  broken  repeatedly  until,  by  adjusting  the  string  tension, 
the  whole  curve  is  deflected  through  3  centimetres  (Fig.  5d). 
Tightening  the  string  reduces  and  slackening  increases  the 
sensitiveness  of  the  instrument. 

6.  A  curve  is  taken  from  the  first  lead. 

7.  The  process  is  repeated  in  the  case  of  leads  //  and 
///.  The  curves  obtained  have  the  correct  amplitude  and  a 
value  of  3  millivolts  to  each  3  centimetres  of  excursion,  or 
1  millivolt  to  the  centimetre  of  excursion. 

For  convenience  of  measurement,  a  screen,  of  millimetre 
lines,  is  placed  immediately  in  front  of  the  photographic 
plate.  The  light,  falling  through  the  screen,  is  intercepted 
by  these  lines  and  the  film  is  ruled  as  the  photograph  is 
taken  (Fig.  5). 

Though  the  steps  taken  in  producing  standardised 
electrocardiograms  may  seem  complicated  and  tedious  in  the 
description,  yet  in  practice  they  become  simple  ;  a  series  of 
curves  from  the  three  leads  should  be  obtained  from  a  single 
subject  within  a  few  moments. 

Checking  the  accuracy  of  standardised  curves. 

The  accuracy  of  excursion  in  a  set  of  curves  from  a 
given  subject  may  be  checked  in  a  simple  manner  by  increasing 

*  In  Fig.   5  c  this  movement  is  very  small. 


10 


Chapter  I. 


the  resistance  in  the  main  circuit 


r--7;rz-rz: " — r~r 


WTTTStTTXXZYJk^i  4  4  t35E3=i      14-4  44+i-i4-H 


Fig.  6.  Six  electrocardiograms  from  lead  /  and  from  a  single 
"  subject,  and  the  six  corresponding  deflections  in  response 
to  a  test  current  Illus-.ratlng  the  distortion  of  curves 
when  the  string  tension  is  too  slack.  As  the  string  is 
slackened  beyond  a  certain  limit  and  the  deflection  time 
(the  time  of  response  to  an  E.M.  F.  of  1  millivolt  over  an 
excursion  of  1  centimetre)increases.J?  and  S  are  materially 
reduced  in  amplitude.  Time-marker  in  thirtieths  of  a 
second  in  this  and  all  other  figures. 


When  curves  have  been 

ig^^gs      taken  from  the  three 

customary    leads    in 

^  A  the  usual  manner,, 
a  large  resistance  is 
placed  in  series  with 
the  string  and 
patient  by  altering: 
the  dial  resistance- 
(B5).  As  a  rule  it  is- 
convenient  to  throw 
in  a  resistance  which 
C  is  approximately 
equivalent  to  that 
teStetSzi  of  the  string  itself.* 
With  this  resistance 
in  circuit  the  same 
procedure  is  fol- 
lowed, the  tension  of 
the  string  being 
suitably  decreased, 
so  as  to  give  the 
original  excursion  of 
3  centimetres  to 
3  millivolts.  The 
second  group  of 
F  curves,  the  one  taken 
with  the  added  re- 
sistance in  series, 
should  be  similar  in 
every  respect  to  the 
original  one. 


wAajflAaJflMMJMM 


*  The  string  resistance  maybe  measured  by  obtaining  a  deflection  of  6  centimetres  with 
3  millivolts,  and  by  placing  such  a  resistance  in  series  with  the  string  as  halvesits  excursion  ;  i.e., 
reduces  it  to  3  centimetres.    The  resistance  of  the  string  and  the  added  quantify  are  then  equal. 


The  Electrocardiographic  Method.  i  1 

Testing  certain  properties  of  the  string. 

If  standard  curves,  and  curves  of  correct  outline,  are 
to  be  obtained,  the  response  of  the  fibre  to  simple  current 
changes  should  be  carefully  examined  from  time  to  time  ; 
for  the  excursion  and  shape  of  an  electrocardiogram  may  be 
modified  by  the  properties  of  the  string.  Supposing  that  an 
E.  M.  F.  of  1  millivolt  is  thrown  into  circuit  (the  patient  being 
disconnected)  and  that  the  tension  of  the  fibre  is  arranged  so 
that  it  gives  an  excursion  of  1  centimetre  ;  the  curve 
obtained  has  an  outline  similar  to  those  shown  to  the  right 
hand  of  Fig.  6.  The  string  moves  when  the  current  enters  it 
and  eventually  takes  up  a  position  1  centimetre  away.  But  in 
arriving  at  the  new  position  it  describes  a  curve.  The 
characters  of  this  curve  are  important.  Fig.  6  shows  six 
electrocardiograms  from  the  same  subject,  and  six  responses 
to  an  E.  M.  F.  of  1  millivolt.  The  curves  differ  because  they 
were  taken  with  different  resistances  in  circuit,  and  con- 
sequently with  different  string  tensions.*  From  above 
downwards  the  added  resistance  was  increased  and  the 
string  was  therefore  slackened.  All  the  curves  were  taken 
with  the  string  at  such  a  tension  that  1  millivolt  gave  1 
centimetre  of  excursion  (see  deflections  to  right  of  strips). 

In  the  first  place,  the  movement  of  the  string  in  response 
to  1  millivolt  should  be  "  dead  beat  "  ;  that  is  to  say,  there 
should  be  no  over-shooting  ;  over-shooting  tends  to  produce 
distortion  of  the  electrocardiograms  by  increasing  the 
amplitude  of  the  initial  deflections.  Over-shooting  is  shown 
in  Fig.  5  (at  b)  at  a  stage  when  the  tension  of  the  fibre  was 
too  great.  In  the  second  place,  the  movement  should  be  of 
sufficient  rapidity.  The  slacker  the  string,  the  more  slowly 
does  it  come  to  rest  in  its  new  position  ;   the  deflection  times 

*  Adding  resistance  to  the  main  circuit  decreases  the  sensitiveness  of  the 
instrument  and  the  string  must  be  slackened  to  compensate  this  decrease  if 
a  constant  excursion  is  to  be  maintained. 


12  Chapter   I. 

for  the  six  strips  of  Fig.  6  are  0-013,  0-023,  0-028,  0-045,  0-060 
and  0-070  second,  respectively,  from  A  to  F.  Now  the 
initial  electric  changes  which  result  from  the  heart  beat  are 
rapid,  and  if  the  quickest  movement  of  which  the  string  is 
capable  is  too  slow  to  follow  these  changes,  an  accurate 
electrocardiogram  is  not  obtained.  Undue  slackness  of  the 
string  distorts  the  curve  and  this  distortion  is  well  illustrated 
by  the  series  of  curves  shown  in  Fig.  6.  As  the  string  is 
slackened,  a  stage  is  reached  when  the  steepest  deflections 
(R,  S)  are  shortened  and  their  upstrokes  and  downstrokes 
are  rendered  more  oblique  ;  once  distortion  appears,  further 
slackening  exaggerates  it  ;  so  that,  as  in  the  last  strips 
of  Fig.  6,  certain  deflections  (such  as  S  and  R)  tend  to 
disappear.  The  electrocardiograms  of  the  first  two  strips 
are  exactly  alike,  these  electrocardiograms  are  accurate  ;  the 
first  change,  a  decrease  in  the  amplitude  of  R  and  S  in  the 
third  strip,  is  seen  when  the  deflection  time  of  the  string  is 
increased  to  0-028  second. 

For  routine  work  the  instrument  and  string  should  be 
tuned,  so  that  while  on  the  one  hand  there  is  no  over-shooting, 
on  the  other  hand  the  deflection  time  does  not  exceed  0-02 
second.  The  best  strings  for  electrocardiographic  work 
are  those  which  give  a  considerable  range,  over  which  these 
two  conditions  are  fulfilled.*  Also  it  is  necessary  that  the 
resistance  of  the  string  should  be  large  compared  with  the 
resistance  of  the  body,  so  that  small  variations  of  the  latter 
do  not  appreciably  affect  the  result.  Strings  having  resistances 
of  about  5,000  ohms  are  suitable. 


*  Intending  students  of  electrocardiography  are  strongly  advised  to 
satisfy  themselves  fully  of  the  adequacy  in  these  respects  of  any  instrument 
with  which  they  propose  to  work. 


13 


Chapter  n. 


THE    PHYSIOLOGICAL    ELECTROCARDIOGRAM. 

The  normal  electrocardiogram  consists  of  a  series  of 
deflections,  some  of  which  are  rapid  and  of  short  duration, 
while  others  are  slow  and  of  longer  duration.  They  have 
been  named  in  a  purely  empirical  fashion,  P,  Q,  R,  8  and  T. 
The  electrocardiogram  opens  with  a  blunt  summit  P,  which 
occupies  presystole,  and  is  due  to  the  activity  of  the  two 
auricles  (Fig.  7  and  8).  Following  upon  this  deflection  the 
string  shadow  either  maintains  the  zero  position  or  dips 
somewhat.  I  speak  of  these  portions  of  the  electrocardiogram 
as  the  "  auricular  complex  "  ;  this  complex  begins  with  the 
upstroke  of  P  and  terminates  at  the  opening  of  the  "  ventri- 
cular complex."  The  latter  varies  in  the  number  of  its 
component  deflections  ;  in  its  full  form  it  comprises  Q,  a 
small  dip,  E,  a  tall  spike,  S,  a  steep  valley  of  variable  depth, 
and  T,  a  broad  blunt  summit.  The  period  occupied  by  all 
these  deflections  is  approximately  that  of  the  ventricular 
systole  with  which  they  are  associated.  The  earliest  sign  of 
actual  contraction  in  the  ventricle  occurs  a  little  after  the 
commencement  of  R,  and  usually  during  its  upstroke.*  The 
contraction  ends  where  T  passes  into  the  horizontal  line  of 
diastole,  or  within  a  few  hundredths  of  a  second  of  this  point. 
These  relations  are  indicated  in  Fig.  8,  which  is  a  simultaneous 
record  of  the  electric  changes  and  the  apical  heart  sounds. 

*  The  electrical  currents  are  not  clue  to  contraction  of  the  muscle  but  to  a 
process  termed  excitation  which  immediately  precedes  actual  contraction. 


14 


Chapter  II. 


Fig.   7.     An  electrocardiogram  from  a  normal  subject,  showing  the  auricular 
summit  (P)    and  the  ventricular  deflections  ( Q,  R.  S  and  T). 

In  this  and  the  remaining  figures,  the  lead  Is  marked  in  the  upper 
left  hand  corner  of  the  figure  ;  the  time,  at  the  bottom,  is  in  thirtieths 
of  a  second,  the  distance  between  the  horizontal  and  parallel  lines 
represents  tenths  of  a  millivolt. 


Fig.  8.  Simultaneous  electrocardiograms  and  heart  sound  curve  from  a 
normal  subject.  The  figure  shows  the  time-relations  of  the  electro- 
cardiogram to  the  beginnings  of  the  1st  and  2nd  heart  sounds.  All 
points  on  any  vertical  line  are  simultaneous. 


Thus,  the  curves  provide  us  with  clear  indications  of 
the  systoles  of  auricles  and  of  ventricles,  and  enable  us  to 
establish,  within  very  small  limits  of  error,  the  time-relations 
of  contraction  in  upper  and  lower  chambers  of  any  given  heart. 

The  initial  ventricular  deflections  ( Q,  R,  S,  or  B,  S,  as 
the  case  may  be)  correspond  to  the  spread  of  the  excitation 


The  Physiological   Electrocardiogram. 


15 


Avave  in  the  ventricle.  This  excitation  wave  is  a  process 
which  precedes  the  actual  wave  of  contraction  by  a  minute 
fraction  of  a  second  ;  it  is  a  preparatory  process  and  the  two 
waves  follow  the  same  course  through  the  heart.  The 
duration  of  the  initial  deflections  may  be  taken  as  a  measure 
of  the  time  during  which  all  parts  of  the  ventricle  are  becoming 
active.  The  final  deflection  (T)  is  produced  by  subsidence 
of  the  ventricular  activity,  and  finishes  at  the  time  when  all 
parts   of  the   ventricle   first   become   quiescent. 


■ — K-T»-\ 


c  :£□= 


jFig.  9.  A  diagram  illustrating  the  theory  of  electric  curves.  It  represents 
a  strip  of  somatic  muscle  connected  to  the  galvanometer  and  stimulated 
to  contract  from  one  or  other  end.  The  deflections,  which  are  shown 
to  the  right,  vary  in  direction  according  to  the  point  at  which  the  con- 
traction originates  and  with  the  relation  of  the  muscle  to  the  electrodes. 


Supposing  that  we  take  a  simple  strip  of  muscle,  the 
fibres  of  which  are  parallel,  and  connect  its  two  ends,  which 
we  will  term  proximal  (p)  and  distal  (d),  to  the  galvanometer. 
If  this  strip  is  stimulated  by  a  single  induction  shock,  say  at 
its  proximal  end  (Fig.  9-4),  then  a  wave  of  contraction  flows 


16  Chapter   II. 

from  p  to  d.  When  the  muscle  at  p  becomes  active,  it  also 
becomes  relatively  negative  to  d,  as  shown  by  the  swing  of 
the  galvanometric  recorder  ;  the  swing  is  in  a  definite  and 
known  direction,  it  is  the  same  as  that  given  when  p  is- 
replaced  by  the  zinc  terminal  of  a  copper-  zinc  couple.  But  the 
wave  passes  to  d  and  as  it  reaches  this  point  it  subsides  at  p. 
The  distal  end  becomes  active  while  the  proximal  end  is- 
resuming  the  quiescent  state  ;  as  an  accompaniment  of  this 
change,  d  becomes  relatively  negative  to  p,  and  the  swing  of 
the  recorder  is  reversed.  Thus  the  whole  electric  effect 
consists  of  two  deflections  which  are  in  opposite  directions,  a 
simple  diphasic  effect.  Now  if  the  stimulus  is  applied  at  the- 
distal  end  (Fig.  9B)  the  direction  of  contraction  is  reversed  ; 
under  these  circumstances  d  first  shows  relative  negativity  and 
later  p  ;  a  diphasic  effect  is  still  obtained,  but  the  directions 
of  swing  are  the  reverse  of  those  seen  when  the  contraction 
travels  from  p  to  d.  It  will  be  evident  that  the  recorded 
curve  will  also  show  reversed  phases  if,  stimulation  being  at 
the  proximal  end,  the  connections  to  the  galvanometer  ar& 
reversed  (Fig.  90). 

The  meaning  of  individual  deflections  in  the  electrocardio- 
gram is  necessarily  a  much  more  complicated  matter  ;  though 
understood  in  great  part,  they  cannot  be  explained  in  any 
detail  in  this  handbook.  I  shall  be  content  to  formulate 
the  chief  conclusions  reached  but  will  defer  these  until  the 
next  chapter.  Meanwhile  certain  fundamental  principles- 
emerge  from  our  simple  experiment.  The  shape  of  the  electric 
curve  is  controlled  (1)  by  the  path  which  the  excitation  wave- 
takes  through  the  tested  muscle,  and  (2)  by  the  lie  of  this 
muscle  in  relation  to  the  leading  off  electrodes.  //  the  wave 
pursues  an  abnormal  course  through  the  heart,  it  will  yield  an- 
abnormal  electrocardiogram.  If  the  points  of  contact,  ivhich  the 
instrument  makes  in  the  body,  are  altered,  the  curve  will  alter 
correspondingly . 


The  Physiological   Electrocardiogram. 


17 


Now  it  is  known  that  all  normal  human  hearts  yield, 
from  a  given  lead,  electrocardiograms  which  conform  to  a  type. 
Although  the  curves  taken  from  no  two  subjects  are  exactly 
alike,  yet  by  experience  we  learn  the  limits  of  variation 
which  are  compatible  with  health. 

The  'physiological  auricular  complex.  P,  the  auricular 
representative,  is  found  as  a  summit*  in  all  normal  and 
young  adult  subjects  and  in  all  leads  ;  it  is  small  and  rarely 
exceeds  2  scale  divisions  in  amplitude  ;  it  is  followed  by  a 
short  line  which  is  horizontal  or  dipping.  Amongst  the 
variations  in  form,  which  P  presents  in  the  normal  subject, 
is    occasional   bifurcation    (Fig.    10).        Auricular   complexes 


mrn  .rrrrmrrrrrrm  r  .  . .  ■  .  i  nnmi  t  rrmn  i  ■  miiilimimimmmmmii  rrrrm 

Fig.   10.     A   normal   electrocardiogram,    showing   a   divided    P   summit ;     a 
prominent   U  summit  occurs  at  the  beginning  of  diastole. 


of  these  forms  are  known  to  express  the  origin  of  the  heart  beat 
at  the  normal  site  of  impulse  formation  and  the  passage  of 
the  wave  through  the  whole  of  the  auricular  tissue  in  definite 
directions. 

The  physiological  ventricidar  complex.  The  variations 
which  are  found  in  the  type  of  the  physiological  ventricular 
complex  are  many.  R  and  T  are  always  present.  Q  and  S 
are  often  absent.  All  the  deflections  vary  in  amplitude  and 
in  shape,  and  in  certain  leads  T  may  vary  in  its  direction. 

*  P  and  R  are  upward  movements  when  the  galvanometric  connections 
are  so  arranged  that  if  the  right  arm  contact  is  replaced  by  the  zinc  terminal 
of  a  copper-zinc  couple,  and  the  left  leg  contact  is  replaced  by  the  copper 
terminal,  an  upward  deflection  results. 


18  Chapter   II. 

The  QRS  group  of  deflections  is  of  short  duration  and  in 
normal  subjects  has  a  total  duration  of  no  more  than  one-tenth 
second.  The  presence  of  a  QRS  group  of  rapid  deflections, 
followed  by  a  slow  blunt  T  deflection,  indicates  that  the 
ventricular  contraction  has  been  propagated  from  normal 
points.  It  has  been  awakened  by  impulses  ivhich  have  traversed 
the  auriculo-ventricular  bundle,  its  main  divisions  and  their 
arborisations. 

Certain  variations  in  the  form  and  amplitude  of  individual 
deflections  require  closer  description,  and  it  will  be  necessary 
to  refer  to  the  leads  from  which  the  curves  are  taken.  We  may 
confine  ourselves  to  those  features  which  are  of  clinical 
importance. 

Curves  from  the  three  leads  of  a  normal  subject  are 
shown  in  Fig.  11.  It  will  be  noticed  that  in  all  R  is  prominent, 
but  that  it  is  most  prominent  in  lead  //,  and  that  T  is  directed 
upwards.  On  the  other  hand  Q  and  S  are  inconstant  in  the 
leads.  This  series  of  curves  may  be  regarded  as  of  average 
type.  In  a  series  of  over  50  young  adult  subjects  the  greatest 
variations  presented  by  serial  leads  are  depicted  in  Fig.  12  and 
13.  The  importance  of  these  extreme  electrocardiograms  will 
be  better  appreciated  when  we  deal  with  pathological  curves 
in  the  next  chapter.  At  present  it  should  be  noticed  that  in 
Fig.  12  R  is  inconspicuous  in  lead  I  and  most  prominent  in 
lead  ///,  while  S  is  most  conspicuous  in  lead  I.  Precisely 
the  reverse  relations  are  shown  in  Fig.  13,  where  R  is  most 
prominent  in  lead  /  and  inconspicuous  in  lead  ///,  while  S 
is  deepest  in  lead  ///.  These  variations  in  amplitude  are 
probably  the  result  of  preponderance  of  the  musculature 
in  right  (Fig.  12)  and  left  (Fig.  13)  ventricles  respectively, 
and  are  extreme  examples  of  the  pictures  which  may  be  found 
in  apparently  healthy  subjects. 

Normal  electrocardiograms  occasionally  exhibit  notching 
of  R  or  S  (Fig.  13)  ;    and  in  lead  III  bizarre  types  of  initial 


The  Physiological  Electrocardiogram. 


19 


deflections  (the   QRS  group)  are  not  uncommon  ;    examples 
are  shown  in  Fig.  14. 

T  is  always  upright  in  young  and  healthy  individuals  in 
lead  II  and  under  normal  conditions,  but  it  is  often  inverted 
in  lead  III  and  may  show  partial  inversion  in  lead  I.  Inver- 
sion in  lead  1 1 1  is  generally  associated  with  the  bizarre  QRS 


-:X±1 


II  I  t  1  II  I  I  I  I  II  I  I  I  I  I  1  II  I  n  I  I  I  I  I  I  I  1  1  1  II  I  I  II  I  I  II  I  ITT-rn 

Fig.  11.  Electrocardiograms  from  the  three  leads  in  a  normal  subject. 
To  illustrate  the  change  in  the  type  of  curve  with  change  of  lead.  Note 
that  R  is  tallest  in  lead  II. 

group  to  which  reference  has  been  made  already  (Fig.  14),  but 
may  occur  with  the  usual  form  of  initial  deflections  (Fig.  12). 

An  additional  deflection  U  is  not  uncommon  and  may  be 
prominent  (Fig.  10).  This  deflection  is  related  to  the  early 
events  of  diastole  and  beyond  this  is  not  understood. 

Standard  curves  from  the  same  subject  are  almost 
identical  in  form  and  amplitude  from  time  to  time.  The 
constancy  is  such,  and  the  variations  in  distinct  subjects  are 
sufficiently  definite,  that  electrocardiograms  might  well  be 

c  2 


20 


Chapter  II. 


-Cp  =        -  7= 

-         ■-,  TTmmuiiuiJhuiiiuiiiuiiiiiiii) 


! 


wA«i«M^  \0^mmam 


.4.i,i.u.u.i.i.ii.u,u4.ui,i.i.4,i.y.i.i.yriri.).i.i.i,y4vUt 


<; 


Fig.   12.     Normal  electrocardiograms  showing  the  tallest  R  in  lead  III  and 
the  shortest  R  and  deepest  S  in  lead  7.     For  comparison  with  Fig.  21. 

Fig.   13.     Normal  electrocardiograms,  showing  the  tallest  R  in  lead  I  and  the 
shortest  R  and  deepest  S  in  lead  III.     For  comparison  with  Fig.  20. 


UIEE^m=T^- 


It.UJJ^U.M.yj.lll.i.lJ.H.U.l.U.Ul.l.l.U.U.U.t.l.U.y.l 


Fig.  14.  Normal  curves  taken  from  lead  117  in  three  different  subjects. 
Illustrating  the  curious  initial  deflections  which  are  sometimes  seen  in 
this  lead.     They  are  often  associated  with  inversion  of  T. 


The  Physiological   Electrocardiogram. 


21 


used  to  identify  the  individual.  Considerable  changes  in 
the  heights  or  directions  of  deflections  in  electrocardiograms, 
taken  from  time  to  time  and  under  similar  conditions,  do  not 
occur  in  health  and  rarely  occur  in  chronic  disease.  An 
observed  change  is  significant  of  altered  function. 

A  certain  familiarity  with  the  limits  between  which  the 
amplitudes  of  deflections  vary  in  health  is  useful  ;  it  is  gained 
by  experience.  Some  idea  of  their  value  may  be  obtained 
from  a  series  of  curves  taken  from  a  number  of  active  students. 
There  were  in  all  59  individuals  from  whom  curves  were 
taken.  The  limits  of  amplitude  for  the  several  deflections  are 
given  in  the  accompanying  table,  which  includes  measurements 
from  52  subjects.    The  measurements  from  seven  subjects  are 


P 

Q 

R 

S 

T 

U 

Lead   I. 

Minimum 

Trace 

0 

1-5 

0 

—0-5 

0 

Average  .  . 

0-52 

0-51 

5-16 

2-06 

1-93 

010 

Maximum 

1 

2-0 

12-0 

6-0 

5-5 

Trace 

Lead 

II. 

Minimum 

Trace 

0 

4-0 

0 

Trace 

0 

Average  .  . 

116 

0-73 

10-32 

2-23 

2-46 

0-16 

Maximum 

1-7 

2-5 

16-5 

4-5 

5-0 

0-8 

Lead 

III. 

Minimum 

Trace 

0 

2-0 

0 

—2-0 

0 

Average  .  . 

0-81 

0-86 

6-61 

1-73 

0-61 

0-06 

Maximum 

1-5 

2-5 

14-0 

4-0 

3-0 

0-3 

not  given  ;  they  were  rejected  from  the  normal  series  for 
various  reasons.  Six  manifested  abnormal  signs  upon  the 
ordinary  physical  examination,  and,  of  these,  four  gave 
electrocardiographic  curves  which  diverged  notably  from 
those  of  the  selected  series.  Only  one  student  in  whom  no 
other   physical   signs    were    obtainable    presented   divergent 


22  Chapter  II. 

electrocardiograms.  Two  subjects  who  gave  normal  electro- 
cardiograms were  found  to  have,  the  one  a  tricuspid  murmur, 
the  other  a  slight  extension  of  the  left  limit  of  heart  dulness. 
These  facts  speak  for  themselves  ;  if  in  any  subject  electro- 
cardiograms which  show  notable  divergence  from  what 
is  regarded  as  normal  are  obtained,  it  is  probable  that  the 
heart  is  abnormal.  But,  on  the  contrary,  if  the  electrocardio- 
grams are  normal  in  form,  it  does  not  follow  that  the  heart  is 
normal. 

Electrocardiographic  curves  are  modified  by  age  ;  the 
chief  change  is  a  decrease  in  the  amplitude  of  T  as  the  subject 
becomes  older.  They  are  also  influenced  by  displacement 
of  the  heart.  They  are  modified  by  exercise,  notably  in  the 
direction  of  an  increase  in  the  amplitude  of  T.  But  these 
factors  materially  influence  the  interpretation  of  pathological 
curves  in  exceptional  cases  only. 


(      23     ) 


Chapter   III 


RHYTHMIC     BUT     ANOMALOUS     ELECTRO- 
CARDIOGRAMS. 

In  the  last  chapter  it  was  shown  that  electric  curves  are 
controlled  by  the  direction  which  the  excitation  wave  takes 
in  the  muscle  yielding  the  record.  Clearly  to  appreciate 
this  principle  and  to  apply  it  constantly  is  the  basis  of 
electrocardiography.  If  the  heart  beat  starts  in  an  abnormal 
focus,  or  if  a  wave,  propagated  from  the  normal  focus, 
subsequently  deviates  from  its  accustomed  paths,  an  anoma- 
lous electrocardiogram  is  the  result.  The  systoles  of  auricle 
or  of  ventricle  may  be  classified  according  to  the  forms  of 
electric  curves  which  they  produce. 

Now,  in  the  natural  heart  beat,  the  wave  is  propagated 
over  auricle  to  ventricle  ;  the  stimulus  is  conveyed  from  the 
first  chamber  to  the  last  through  the  auriculo-ventricular 
bundle  ;  thence  it  spreads  through  the  two  main  divisions 
of  this  bundle  and  is  distributed  to  the  right  and  left  ventricle 
through  the  arborisations  and  basketworks  of  Purkinje  cells. 
In  these  circumstances  the  systole  which  follows  yields  an 
electrocardiogram  conforming  to  a  recognised  type  ;  the 
familiar  deflections,  Q,  B,  S  and  T  are  produced.  This 
type  of  electrocardiogram  is  only  seen  when  the  systole  to 
which    it    corresponds   is   provoked    by   an   impulse    arising 


24  Chapter  III. 

above  the  division  of  the  A-V  bundle — an  impulse  which  I 
distinguish  as  supraventricular — and  it  is  limited  to  responses 
of  the  ventricle  to  supraventricular  impulses  which  descend 
all  the  normal  channels.  Thus,  if  the  ventricle  responds  to 
an  impulse  generated  in  its  own  walls,  the  electrocardiogram 
is  abnormal.  (See  Chapter  V.  on  Premature  Contractions.) 
The  curve  is  also  abnormal  if  a  supraventricular  impulse 
is  distributed  to  the  ventricle  in  an  unusual  manner,  as  may 
happen.  For  in  the  first  instance,  and  in  the  second,  the 
course  which  the  resultant  wave  takes  in  the  ventricular 
walls  deviates  from  the  normal. 

The  constitution  of  the.  ventricular  complex. 

When  a  supraventricular  impulse  (for  example,  the  normal 
impulse),  on  passing  to  the  ventricles,  enters  the  normal 
field  of  reception,  it  reaches  the  two  ventricles  simultaneously. 
Each  ventricle  possesses  a  complete  and  separate  system  of 
distributing  fibres  (see  Fig.  15,  top  diagram).  Each  ventricle 
yields  its  own  electric  currents  and  each,  while  beating 
normally,  yields  a  distinctive  curve.  Up  to  a  point  the 
forms  of  the  curves  distinguishing  the  normal  systole  of 
right  and  left  ventricles,  respectively,  are  known  to  us.  It 
is  for  the  student  of  electrocardiography  to  become  thoroughly 
familiar  with  these  types.  In  Fig.  15  is  a  diagram  of  the 
ventricles,  seen  in  section,  and  of  the  auriculo-ventricular 
bundle  and  its  ventricular  connections.  The  septum  of  the 
ventricles  forms  a  saddle  across  which  the  dividing  bundle 
sits  astride.  If  the  right  division  of  the  bundle  is  transected 
below  its  origin  (as  at  B1)  the  normal  impulse  no  longer 
travels  through  it,  but  passes  solely  through  the  left  stem. 
The  distribution  of  the  impulse  is  faulty,  but  it  is  only  faulty 
in  so  far  as  the  right  ventricle  is  concerned  ;  it  is  distributed 
to  the  left  chamber  in  a  perfectly  normal  fashion.  The 
curves  which  this  partial  distribution  yields  are  shown  in  the 


Anomalous  Electrocardiograms. 


25 


Fig.  15.       A    diagram    of    the    ventricles    seen   in    section    and   of    the 
auriculo-ventricular  bundle  and  its  branches. 

A  lesion  of  the  bundle  division  at  A''  forces  the  natural  impulse  to  descend  solely  through  the 
right  division,  the  supply  of  the  right  ventricle.  The  corresponding  electrocardiograms  are 
characteristic,  and  are  not  dissimilar  in  form  to  those  obtained  by  stimulating  the  right  ventricle 
at  A.  A  lesion  of  the  right  bundle  division  at  5'  confines  the  descending  impulse  to  the  path  of 
the  left  division.  The  corresponding  curves  are  characteristic  and  are  not  dissimilar  in  form  to 
those  obtained  by  stimulating  the  left  ventricle  at  B. 

Below  the  diagram  are  two  series  of  curves,  arranged  vertically  and  corresponding  to  leads  1 
and  27"/.  The  top  curve  in  each  series  is  the  levogram,  obtained  when  the  right  bundle  division 
is  damaged;  the  middle  curve  in  each  series  is  the  dextrogram.  obtained  when  the  left  bundle 
division  is  damaged.  The  bottom  curves  represent  the  initial  phases  of  the  normal  electro- 
cardiogram and  the  diagram  it  arranged  to  show  that  these  initial  phases  are  the  algebraic  product  S 
•of  the  levogt'am  and  dextrogram.  In  the  series  from  lead  2"  I  have  inserted  the  amplitudes  of  the 
curves  where  they  cross  the  common  vertical  lines,  marking  them  as  +  or  -  quantities  according 
as  the  deflection  is  up  or  down.  Thus  Q  (  -  2)  is  the  result  of  a  similar  dip  (-  2)  in  the  levogram  ; 
R  (15>  is  the  product  of  the  small  spike  (5)  in  the  dextrogram  and  of  the  rising  levogram  (10). 


26  Chapter  III. 

diagram  (L  L),  and  these  curves  in  their  initial  phases  (while 
the  excitation  is  confined  to  the  left  ventricle)  represent  the 
currents  normally  formed  in  the  left  ventricle.  In  lead  / 
the  curve  comprises  a  small  downward  phase,  a  large  upward 
phase  and  a  final  and  sustained  downward  phase.  In  lead 
///  the  curve  comprises  a  small  upward,  a  large  downward 
and  a  final  and  sustained  upward  phase.  Because  these 
curves  correspond  in  their  initial  phases  to  the  natural 
systole  of  the  left  ventricle,  I  call  them  levograms.  If,  on  the 
other  hand,  the  left  bundle  division  is  divided  the  impulse 
is  conveyed  solely  to  the  right  ventricle;  but  this  distribution 
in  so  far  as  it  affects  the  right  ventricle,  is  again  normal. 
The  corresponding  curves,  which  I  term  dextrograms ,  are 
shown  in  the  diagram  (D  D).  The  curve  of  lead  /  comprises 
a  small  upward  phase,  a  large  downward  phase  and  a  final 
upward  phase  ;  in  lead  1 1 1  it  comprises  a  small  downward 
phase,  a  large  upward  phase  and  a  final  downward 
phase. 

Now  the  levogram  and  dextrogram  are  not  only  of 
intrinsic  clinical  importance,  but  they  also  show  us  how  the 
normal  electrocardiogram  is  constituted.  I  have  indicated 
that  in  so  far  as  their  initial  phases  are  concerned  they 
represent  the  normal  events  in  the  left  and  right  ventricle 
respectively.  Each  ventricle  forms  its  own  currents  and  it 
is  the  combination  of  the  two  effects  which  constitutes  the 
normal  curve  or  bigram.  In  the  left  hand  series  of  curves 
of  Fig.  16  the  levogram  and  dextrogram  of  lead  I  are 
diagrammatised.  Summate  the  initial  phases  of  these 
two  curves,  add  them  together  algebraically,  and  the  result 
is  the  initial  phases  Q,  R  and  S  of  the  normal  heart  beat. 
A  similar  summation  of  the  levogram  and  dextrogram  in 
lead  III  will  yield  the  normal  curve  in  lead  ///.  Study 
of  this  diagram  will  show  that  in  human  electro- 
cardiograms : — 


Anomalous  Electrocardiograms .  27 

In  lead  I     ,l  Q  "  is  a  left  ventricular  event. 

"  E  "  is  mainly  a  left  ventricular  event. 
"  S  "  is  a  rigr/zi  ventricular  event. 
While  in  lead  1 1 1  "  Q"  is  a  right  ventricular  event. 

"  E  "  is  mainly  a  right  ventrictdar  event. 
"$.'-'  is  a  left  ventricular  event. 

That  these  conclusions  are  important  will  become  clear 
when  the  curves  corresponding  to  hypertrophy  of  the 
ventricles  are  described. 


Aberrant  beats. 

I  term  those  beats  of  the  ventricle  aberrant  which,  pro- 
pagated from  supraventricular  impulses,  are  distributed  in  a 
partial  or  faulty  fashion  ;  these  aberrant  beats  are  f recently 
discovered  in  clinical  electrocardiograms.  Just  as  the 
functions  of  the  main  stem  of  the  A-V  bundle  are  often 
defective  in  the  human  subject  (see  Chapter  IV.),  so  also  are 
those  of  its  individual  branches.  The  types  of  electrocardio- 
gram representing  deficient  conduction  in  the  main  divisions 
of  the  bundle  are  illustrated  by  actual  examples  in  Fig.  16 
and  17  (and  have  been  in  part  described  in  reference  to 
Fig.  15).  The  natural  auriculo- ventricular  sequence  is 
maintained,  that  is  to  say,  each  ventricular  beat  is  preceded 
by  an  auricular  one  ;  the  ventricular  complexes  are  alone 
abnormal.  The  common  features  of  the  ventricular  curves 
are  the  exaggerated  amplitude  of  excursion*  and  the  prolonga- 
tion of  the  initial  phases.  The  deflections  which  replace  the 
usual  QES  group  (initial  deflections)  have  a  total  duration 
exceeding  a  tenth  of  a  second  and  comprise  more  than  a 
third  of  the  whole  complex.     When  the  right  branch  is  at 

*  The  amplitudes  are  often  much  greater  than  in  the  curves  chosen  for 
illustration. 


28 


Chapter  III. 


Levograms. 


f*mi&~-- 


.el. 


■  •  n  r  i  r  •  •  t  • ' 


MUMMUMM 


DeXTRO  GRAMS. 


Fig.  16.  Curves  from  the  three  leads,  evidencing  functional  defect  of  the 
right  di vision  of  the  auriculo -ventricular  bundle.  Note  the  long  duration 
of  the  initial  phases  and  the  large  amplitude  in  leads  I  and  ///. 

Fig.  17.  Curves  from  the  three  leads,  evidencing  functional  defect  of  the  left 
division  of  the  auriculo-ventricular  bundle.  The  directions  of  the 
deflections  are  the  reverse  of  those  of  the  last  figure,  in  leads  /  and  III 


fault  the  first  chief  deflection  is  a  broad  summit  R1  in  lead  /, 
a  deep  and  broad  depression  S1  in  lead  III  (Fig.  16).  Each 
of  these  phases  is  followed  by  a  sustained  and  very  prominent 
phase  T1  which  is  of  opposite  sign  to  the  first  chief  deflection 
in  the  same  lead  ;  it  is  directed  down  in  lead  /  and  up  in 
lead  ///.  When  the  left  branch  is  at  fault  the  pictures  are 
reversed  (Fig.  17).  A  deep  depression  S1  is  followed  by  an 
upright  and  prominent  T1  in  lead  /  ;  a  broad  summit  R1 
is  followed  by  a  downward  directed  T1  in  lead  ///.  In 
addition  to  these  deflections,  a  dip  {Ql)  may  appear  to  a 
variable  extent  in  lead  /  of  the  levogram  and  in  lead  III  of 


Anomalous  Electrocardiograms. 


29 


i  t  I  I  *  i  i,  I  *  *  i  , 


Fig  18. 


T^rnrre  ..........  r-.  ..............  . 


Fig.   19. 


Fig. 


Fig. 


IS.  Curves  taken  from  the  three  leads  in  a  case  of  aortic  disease  during 
a  febrile  attack.  They  show  defective  conduction  along  the  right 
division  of  the  auriculo-ventricular  bundle  (see  Fig.  16). 

19.  Curves  from  the  same  patient,  taken  a  day  later  and  during  the 
subsidence  of  the  fever.  The  ventricular  portions  of  the  curves  have 
changed  profoundly  ;  there  is  now  no  evidence  of  bundle  defect,  but  of 
preponderance  of  the  left  ventricle. 


the  dextrogram,  while  a  diminutive  summit   B1  may  open 
lead  III  oi  the  levogram  and  lead  /  of  the  dextrogram.* 

The  value  of  these  electrocardiograms  as  signs  of  disease 
is  great,  for  damage  of  the  bundle  divisions  is  to  be  identified 
by  them,  and  by  them  only.f  The  pathology  of  the  lesions 
is  similar  to  that  of  auriculo-ventricular  heart-block,  which  is 
frequently  coincident.  As  a  permanent  condition,  damage 
of  a  bundle   branch    speaks  for  a  lesion  in  this   situation, 

*  The  curves  of  lead  II  are  often  similar  to  those  of  lead  III  in  lesions  of 
the  right  division,  but  in  lesions  of  neither  division  are  they  so  characteristic 
as  in  leads  /  and  ///. 

t    A  reduplication  of  the  first  heart  sound  is  a  frequent  but   inconstan 
association. 


30  Chapter  111. 

though  the  latter  is  usually  but  a  local  expression  of  wide- 
spread mischief  in  more  silent  areas.  As  a  temporary 
condition  it  results  from  an  acute  or  subacute  process,  an 
invasion  of  the  myocardium  by  an  infective  agent  or  poison. 
Such  was  the  probable  explanation  in  the  case  from  which 
Fig.  18  and  19  were  taken.  Admitted  to  hospital,  he  was 
found  to  have  an  aortic  lesion  ;  the  temperature  was  100°, 
but  there  were  no  other  clinical  signs  of  infection.  The 
electrocardiograms  (Fig.  ]  8}  showed  deficient  conduction  in 
the  right  branch  of  the  bundle,  a  deficiency  which  passed 
away  as  the  fever  subsided  (Fig.  19).  The  electrocardiogram 
provided  the  sole  evidence  of  an  acute  myocardial 
involvement. 

That  the  sign,  as  a  persistent  sign,  is  frequent  in  heart 
cases  we  know  ;  as  a  transient  sign  it  is  probably  more 
frequent  than  we  suspect.  The  right  division  is  much  the 
commoner  to  be  affected,  probably  because  it  runs  a  much 
longer  course  as  an  isolated  strand.  Curiously,  a  defect  of  this 
division  is  often  associated  with  aortic  disease.  The  death 
rate  amongst  patients  who  exhibit  it  is  extraordinarily  high. 

Preponderance  of  left  or  right  ventricle. 

Before  discussing  the  electrocardiograms  associated  with 
hypertrophy  of  the  ventricles  it  will  be  convenient  to 
particularise  in  respect  of  terms.  Normally  the  separated 
ventricles  when  weighed  show  a  certain  mass  relation  to  each 
other  ;  the  left  ventricle  in  the  average  weighs  approximately 
1*8  times  as  much  as  the  right.  In  instances  of  hypertrophy 
of  the  heart  it  is  usual  to  discover  an  increase  in  the  weight 
of  both  ventricles,  pure  unilateral  hypertrophy  as  a  mani- 
festation of  disease  being  rare  ;  but  although  there  is  this 
bilateral  hypertrophy,  one  ventricle  is  often  involved  to  a 
greater  extent  than  the  other  and  the  normal  weight  ratio 
between   the   two   ventricles   is   then   disturbed.        It   is   an 


Anomalous  Electrocardiograms.  31 

altered  ratio  and  that  alone  which  conditions  the  form  of 
the  electrocardiograms  to  be  described. 

If  I  were  to  speak  of  certain  changes  in  the  electrocardio- 
gram and  were  to  relate  them  to  hypertrophy  of  one  ventricle, 
I  might  be  understood  to  mean  that  the  other  ventricle  is  not- 
enlarged,  I  should  certainly  infer  that  the  heart  as  a  whole 
is  increased  in  weight.  To  avoid  these  difficulties  and  to  give 
greater  precision  to  the  description,  I  speak  of  preponderance 
of  a  ventricle,  and  imply  simply  that  the  ventricle  in  question 
is  weightier  as  compared  to  the  other  ventricle  than  it  is  in 
the  average  healthy  adult.  The  point  which  it  is  desired  to 
emphasise  is  that  the  term  preponderance  is  employed 
irrespective  of  the  weight  of  the  whole  heart. 

I  shall  be  dealing,  though  not  exclusively,  with  instances 
■of  actual  hypertrophy,  confined  may  be  to  one  chamber, 
but  more  usually  affecting  the  two  chambers  unequally. 
Speaking  of  hypertrophy,  there  are  certain  preliminary 
considerations  which  I  would  impress  upon  my  reader. 
While  purely  mechanical  influences  undoubtedly  influence 
the  distribution  of  the  mass  of  ventricular  muscle,  yet 
hypertrophy  often  exists  where  there  is  no  reason  to  suspect 
-antecedent  alterations  of  the  fluid  pressures  in  the  chambers, 
and  where  the  degree  of  hypertrophy  in  a  given  chamber 
cannot  legitimately  be  ascribed  to  an  increase  in  the  burden 
which  that  chamber  may  be  supposed  to  have  borne. 
Unquestionably  there  are  causes  of  ventricular  hypertrophy, 
and  of  massive  hypertrophy,  which  are  still  unknown  to  us  ; 
I  would  even  go  so  far  as  to  say  that  the  chief  cause  of 
hypertrophy  is  still  unknown,  and  that  we  are  unaware  of  the 
extent  to  which  such  unrecognised  factors  may  be  responsible 
for  the  hypertrophy  associated  with  valvular  disease.  If 
electrocardiograms  are  sometimes  obtained  which  point  to 
preponderance  of  one  chamber,  while  the  clinical  signs 
display  a  valve  lesion  usually  associated  with  hypertrophy 


32  Chapter  III. 

of  the  other  chamber,  or  even  reliable  signs  of  hypertrophy  in 
the  other  chamber,  the  electrocardiographic  signs  are  not  to 
be  neglected.  Providing  that  the  heart  is  not  materially 
displaced,  the  electric  curves  are  to  be  accepted.  If 
hypertrophy  of  the  left  ventricle  is  anticipated  from  the 
valve  lesion,  or  if  reliable  clinical  signs  of  left  hypertrophy 
are  present,  and  yet  the  curves  of  right  preponderance  are 
obtained,  then  the  right  ventricle  is  also  hypertrophied 
and  to  an  even  greater  extent  than  the  left.  Or  if,  in  the 
same  conditions,  the  curves  show  no  sign  of  left  or  of  right 
preponderance,  then  the  right  ventricle  is  hypertrophied  to 
as  great  an  extent  as  the  left. 

The  electrocardiograms  associated  with  preponderance  of 
the  left  ventricle  are  curves  in  which  there  is  a  predominance 
of  the  levogram  ;  they  are  illustrated  by  Fig.  20.  The 
amplitude  of  R  is  greatest  in  lead  /  and  is  least  in  lead  III  \ 
S  is  greatest  in  lead  III  and  is  inconspicuous  in  lead  /  ; 
Q  is  most  prominent  in  lead  /.  Reference  to  Fig.  15  wilL 
show  why  this  should  be,  for  the  deflections  which  are 
exaggerated  in  left  ventricular  preponderance  are  the 
deflections  derived  entirely  or  in  chief  part  from  the  levogram 
(see  Table  on  page  27).  As  is  to  be  expected,  the  curves 
of  left  preponderance  are  to  be  seen  most  frecpiently  in 
association  with  aortic  disease,  heightened  blood  pressure^ 
and  in  the  senile  heart.  In  preponderance  of  the  right  ventricle 
(Fig.  21)  the  dextrogram  predominates,  S  is  exaggerated  in 
lead  /  and  is  shortest  in  lead  ///,  R  has  its  greatest 
amplitude  in  lead  ///  and  is  inconspicuous  or  absent  in  lead  Iy 
Q  is  most  in  evidence  in  lead  ///.  The  deflections  which 
are  exaggerated  are  those  derived  from  the  dextrogram. 
The  curves  of  right  preponderance  are  obtained  in  an 
exaggerated  form  from  cases  of  congenital  pulmonary 
stenosis  and  they  are  obtained  in  nearly  all  uncomplicated 
cases    of    advanced    mitral    stenosis.     The    constancy    with 


Anomalous  Electrocardiograms . 


33 


which  they  are  obtained  from  the  new-born  child  (Fig.  22 
and  23)  is  most  notable,  for  in  the  new-born  child  the  right 
ventricle  is  as  heavy  as  the  left.  In  children  the  healthy 
adult  types  of  electrocardiogram  become  established  between 
the  ends  of  the  second  and  third  month  of  extrauterine  life  ; 
it  is  at  the  same  period  that  the  normal  weight  ratio  between 
right  and  left  ventricles  becomes  established. 


utn  1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1  m  1 1 1 1 |,^i ^.»,i  t  f  f  jjjfi 


2^3£ 


Fie.   20. 


iillM  II  1  I  I  I  I  I  H  I  I  I  I  I  I  I  J  I  1  I  I  I  I  I  I  I  I  I  I  I  I  I  I  1  i  I  I  I 

.ZJCZAL.ZZ1T1.- 


■«w<>v(i*ii(ti(aivi«(ti*i«**i(icfii*(«ti(i« 


Fie.   21. 


Fig.  20.  Curves  from  the  three  leads  in  a  case  of  aortic  disease  showing 
preponderance  of  the  left  ventricle.  R  is  tallest  in  lead  I  and  shortest 
in  lead  III,  while  S  is  deepest  in  lead  III. 

Fig.  21.  Curves  from  the  three  leads  showing  preponderance  of  the  right 
ventricle.  Note  that  there  is  but  a  trace  of  R  in  lead  /  and  that  S  is  very 
deep  ;    also  that  R  is  tallest  in  lead  ///,  while  S  is  small. 

Between  the  curves  of  ventricular  preponderance  and 
the  curves  corresponding  to  lesions  of  the  A-V  bundle 
divisions  there  are  naturally  many  points  of  similarity  ;  there 
are  differences  also.  The  directions  of  the  chief  initial  phases 
are  the  same  in  the  two  groups  ;  but  in  instances  of  the 
ventricular    preponderance,     the     duration     of    the     initial 


154 


Chapter  III. 


deflections  is  in  the  average  much  less  ;  it  does  not  usually 
reach  a  tenth  of  a  second  and  does  not  comprise  as  much 
as  a  third  of  the  whole  complex.  In  exceptional  instances 
of  preponderance,  however,  where  one  ventricle  is  enormously 
increased  as  compared  to  the  other,  the  initial  deflections  of 
the  corresponding  electrocardiograms  are  prolonged  and 
then  they  may  be  indistinguishable  from  those  seen  in  lesions 
of  the  bundle  divisions.     In  such  cases  the  distinguishing 


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Fig.  22.  Curves  from  a  child  two  hoiirs  after  birth.  The  relative  heights 
and  depths  of  the  peaks  is  such  as  is  expected  where  there  is  preponderance 
of  the  right  ventricular  muscle. 

Fig.  23.  Curves  from  the  same  child,  but  six  weeks  later.  The  right-sided 
preponderance  is  not  evidenced  by  these  curves  to  nearly  the  same  extent. 


feature  is  discovered  in  the  direction  of  the  final  deflections. 
In  lesions  of  the  bundle  divisions,  the  final  deflection  T1  in 
leads  /  and  III  is  always  of  opposite  sign  to  the  chief 
initial  deflection  and  is  of  unusual  amplitude  ;  in  cases  of 
preponderance  this  rule  does  not  hold  good,  moreover  the 


Anomalous   Electrocardiograms.  35 

final  deflections  T  are  not  more  pronounced  in  amplitude 
than  are  they  in  health.  The  two  series  of  curves  are  well 
contrasted  in  Fig.  18  and  19,  both  series  being  taken  from  the 
same  patient. 

Inversion  of  "  T  ." 

In  young  and  healthy  adults  the  final  deflection  T  is 
always  upright  in  lead  //,  almost  always  upright  in  lead  /, 
but  often  inverted  in  lead  ///.  Inversion  of  T  in  lead  // 
may  be  provoked  transiently  by  digitalis.  As  a  persistent 
phenomenon  it  is  seen  from  time  to  time  in  elderly  subjects  ; 
it  is  most  commonly  displayed  by  patients  in  whom  there 
are  abundant  signs  of  grave  myocardial  disease  (Fig.  19  and 
95).  Whether  it  may  be  regarded  as  serviceable  in  prognosis 
is  for  the  future  to  decide.  Most  of  the  patients  in  whom  I 
have  seen  it  have  already  succumbed,  but  one  patient  is  still 
alive  and  in  no  worse  health  than  when  I  obtained  this  sign 
from  him  seven  years  ago. 


»  2 


(      36     } 


Chapter  IV. 


AURICULO-VENTRICULAR    HEART-BLOCK,    ETC. 

Partial  heart-block. 

The  chambers  of  the  normal  heart  contract  in  orderly 
sequence  ;  each  impulse,  generated  in  the  neighbourhood 
of  the  sino-auricular  node,*  courses  through  both  auricles, 
and  arriving  at  the  auriculo-ventricular  bundle,  the  specialised 
structure  which  unites  auricles  and  ventricles,  is  transmitted 
to  the  ventricles  and  these  respond  to  it.  There  is  an 
appreciable  delay  in  this  transmission  ;  the  auricle,  as  we 
know,  contracts  before  the  ventricle  ;  and  the  interval 
between  the  onsets  of  systole  in  auricle  and  ventricle 
indicates  the  length  of  this  transmission  time.  The 
electrocardiogram  measures  this  interval  more  accurately 
than  any  other  method  which  we  possess.  The  interval  may 
be  gauged  as  accurately  in  the  human  subject  to-day  as  in 
an  experiment  upon  an  animal  in  which  auricle  and  ventricle 
are  laid  bare.  The  measurement  is  taken  from  the  com- 
mencement of  P,  the  auricular  summit,  to  the  commencement 
of  the  ventricular  complex  ;  as  a  rule  R  is  used  for  the  sake 
of  uniformity,  but  Q,  which  is  often  the  first  ventricular 
deflection,  may  be  adopted  if  it  is  thought  desirable.     The 

*  A  special  structure  in  the  mammalian  heart  and  situated  at  the  opening 
of  the  superior  vena  cava.  It  gives  rise  to  the  normal  heart  rhythm,  and  in 
virtue  of  this  function  I  term  it  the  "  pacemaker*" 


Auriculo-ventricular   Heart-block,  etc. 


37 


P-R  interval,  as  it  is  termed,  varies  in  normal  subjects 
between  0*12  and  0*18  second  in  length.  Prolongation  beyond 
0*2  second  is  never  found  in  healbhy  hearts.  Such  prolonga- 
tion represents  the  first  stage  of  heart-block.  Fig.  24  illustrates 
the  condition  described  ;  in  it  the  P-R  interval  measures 
0*32    second.       The    sole    disturbance,    as    shown    bv    the 


i  i t-i-i'n n  i'u  n f«  n'n 1 14 n  m  1 1 4 1 1 iVi  '-in  n  n'm-n i n^Tti ni-i  i  i ii 1 1 1 1  n  n  1 1 1 1 1 1  n 1 1 1  m i n n- 

Fig.  24.  An  electrocardiogram  from  a  case  of  subacute  cystitis,  showing 
prolongation  of  the  P-  R  interval  to  0-32  second.  Time-marker  in  thirtieths 
of  a  second. 


Fig.   25.     From   the   same   case,    showing    a   single    dropped   beat. 

electrocardiogram,  is  an  increase  of  the  interval  named  ; 
individual  auricular  and  ventricular  summits  are  of  normal 
outline.  The  heart  which  manifests  this  change  beats 
regularly.* 

The  next  phase  in  the  progress  of  heart-block  is  termed 
the  stage  of  "  dropped  beats,"  where,  from  time  to  time,  an 
auricular  systole  provokes  no  ventricular  response.  The 
electrocardiograms  show  perfectly  regular  and  normal 
auricular  summits    P,   and  most   of  them   are  followed  by 

*  Prolongation  of  the  P-R  interval  in  patients  who  suffer  from  fainting 
attacks  or  fits  suggests  that  these  attacks  are  of  cardiac  origin. 


38  Chapter  IV. 

ventricular  complexes  ;  but  here  and  there  a  ventricular 
complex  is  missed  and  the  auricular  peak  stands  isolated. 
This  is  one  of  the  causes  of  so-called  pulse  "  intermittence." 
A  simple  example  of  the  condition  is  shown  in  Fig.  25  ; 
measurement  will  show  that  the  auricular  contractions  are 
equidistant,  while  the  intervals  between  the  ventricular  beats 
vary.  An  interval,  of  almost  double  the  usual  length, 
separates  two  of  the  ventricular  contractions  ;  the  long 
cycle  is  not  exactly  twice  the  length  of  the  usual  cycle, 
because,  as  the  figure  shows,  the  P-R  interval  which  ends  the 
long  cycle  is  shorter  than  the  remainder  ;  the  ventricular  beat 
which  stands  at  the  commencement  of  the  restored  rhythm 
has  been  moved  a  little  to  the  left  of  its  natural  position, 
slightly  shortening  the  cycle  to  the  left  of  it  and  slightly 
widening  the  cycle  to  the  right  of  it.  All  the  remaining  P-R 
intervals  are  of  equal  length  and  increased  duration.  This 
distribution  of  the  ventricular  beats  is  characteristic  of 
the  irregularity.  Fig.  27  and  28  exemplify  the  same 
phenomena.  In  Fig.  27  ventricular  silences  occur  after 
each  third  or  fourth  auricular  cycle.  The  analysis  of  a 
curve  of  this  kind  is  readily  accomplished  :  consider  the 
central  group  of  three  ventricular  beats  ;  the  first  is  preceded 
by  an  unmistakable  auricular  contraction  (P5)  ;  it  lies 
in  a  long  diastole.  A  similar  auricular  contraction  (P9)  is 
found  at  the  end  of  the  next  long  diastole.  The  remaining 
auricular  contractions  are  discovered  on  attending  closely 
to  the  shapes  of  the  P  summits.  P3,  P4  and  P5  have 
different  forms  ;  the  first  and  last  are  split  ;  P4  is  tall  and 
pointed.  The  P  summits  have  different  forms  because  P 
summits  fall  with  them.  If,  in  this  curve,  we  take  a  distance 
of  6  time-marks  from  the  commencement  of  an  R  summit 
and  measure  to  the  right,  we  shall  always  arrive  at  the  apex 
of  the  corresponding  P  summit,  for  the  length  of  systole  is 
constant  in  the  curve.       That  the  remaining  summits  are 


Auriculo-ventricular  Heart-block,  etc. 


39 


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40  Chapter   IV. 

auricular  is  proved  by  measuring  the  intervals  between  them  ; 

P5  and  P6  are  separated  by  the  same  interval  as  P8  and  P9. 

The  distance  between  P6  and  P8  is  exactly   twice   as  great, 

and  the  intermediate  point  lies  on  the  summit  of  T4.      T4  and 

P7  are  blended  ;    the  two  summits  superimpose  accurately, 

whence  the  tallness  of  this  peak.     A  perfectly  regular  series 

of   auricular   summits,   therefore,   is   present   in   the   curve  ; 

on  the  other  hand  the  ventricle  beats  irregularly.     Yet  the 

contractions     in     upper     and   lower    chamber    are    related, 

for  the  events  are  repeated.     The  fifth  auricular  contraction 

(P5)    yields    the    third    ventricular      response      (P3)  ;      the 

succeeding  auricular  contractions  (P6  and  P7)  also  stimulate 

the  ventricle   (P4  and   P5),  but  after  progressively  greater 

intervals  ;    the  last  auricular  contraction  of  the  group  (P8), 

falling  far  back  into  ventricular  systole  as  it  does,  stands 

isolated,  and  the  ventricular  silence  before  the  same  events 

are    repeated.     The   shortening    of   the    P-R   interval    after 

the  long  diastole  in  this  figure  and  in  Fig.  25  results  from 

rest  and  the  consequent  recovery  of  the  conducting  tissues  ; 

subsequently,  as  impulse  after  impulse  is  transmitted,  these 

tissues   show   greater   and   greater  fatigue,   until  eventually 

a   stimulus  fails   to   pass.     A  beautiful  example   of  similar 

events  is  portrayed  in  Fig.  28.     The  analysis  proceeds  along 

parallel  lines   to   that   just   given  and  is   portrayed  by  the 

diagram    of    auricular    and    ventricular    contractions    ruled 

upon  the  figure  ;    but  the  fatigue  comes  more  slowly  and 

only  two  ventricular  silences  are  to  be  seen.     Fig.   27  has 

a  companion  curve,  namely  Fig.  26.     The  two  curves  were 

taken  from  the  same  patient.     Fig.  26  was  obtained  shortly 

after  exercise  ;  it  is  noteworthy  that  all  ventricular  irregularity 

was    abolished    by    this    exercise,    while    the    auricular   rate 

was  somewhat  increased.     The  interpretation  of  this  curve 

is  not  evident  at  first  sight  ;    R  and  S  are  readily  identified, 

but  T  seems  double.     The  first  of  the  twin  peaks  represents 


Auriculo-ventricular   Heart-block,  etc.  41 

an  auricular  systole  in  each  cycle  ;  this  is  known  by  measure- 
ment of  the  interval  between  R  and  the  summits  in  this 
figure  and  in  Fig.  27.  The  relations  are  the  same  as  those 
shown  by  P8  and  T5  of  the  second  figure.  Thus  the  P-R 
interval  throughout  Fig.  27  shows  great  prolongation  ; 
the  auricular  systoles  do  not  fall  in  presystole  or  even  in 
early  diastole,  but  they  coincide  with  the  preceding  ventricular 
systoles.  In  human  electrocardiography  it  is  safe  to  assume 
that,  if  T  shows  bifurcation,  it  is  complicated  by  an  auricular 
complex  ;  and  this  general  statement  applies  equally  to 
individual  T's  and  to  a  series  of  T's  so  deformed.  Fig.  29  also 
shows  partial  heart-block.  Here  there  is  no  difficulty  in 
picking  out  the  auricular  contractions,  for  they  have  the  form 
which  they  so  commonly  assume  in  mitral  stenosis.  In  the 
earliest  part  of  the  figure  the  response  to  each  third  auricular 
beat  fails  ;  in  the  last  part  of  the  figure  what  is  known  as 
2  :  1  heart-block,  in  which  alternate  auricular  impulses 
alone  yield  responses,  is  present.  The  figure  demonstrates 
the  same  variation  in  P-R  intervals  which  has  been  referred 
to  in  discussing  the  other  figures.  A  long  diastole  is  followed 
by  a  short  P-R  interval  and  a  short  diastole  by  a  long  one, 
according  to  the  preceding  period  of  rest. 

Partial  heart-block  is  of  great  clinical  importance, 
though  it  is  not  within  the  scope  of  the  present  book  to 
discuss  it  from  this  standpoint.  This  has  already  been 
attempted  in  Clinical  Disorders  of  the  Heart  Beat.  As 
a  permanent  condition  it  tells  us  of  chronic  myocardial 
damage  ;  as  a  temporary  event,  it  speaks  of  an  acute  heart 
lesion  or  poisoning.  It  will  be  sufficient  if  I  briefly  relate 
the  histories  of  the  curves  now  presented.  Fig.  24  and  25 
were  taken  from  a  young  boy  admitted  to  hospital  for 
subacute  cystitis,  resulting  from  an  infection  by  an  organism 
of  the  coli  group.  While  lying  in  bed  for  observation  he 
developed  an  occasional  irregularity  of  the  pulse  to  which 


42  Chapter  IV. 

little  significance  was  attached.  When  specially  examined r 
the  heart-block  was  discovered,  and  it  became  clear  that  the 
heart  was  invaded,  either  by  the  organism  itself,  or  by  the  pro- 
ducts of  its  digestion.  Appropriate  treatment,  applied  to  the 
bladder,  was  followed  not  only  by  subsidence  of  the  cystitis^ 
but  eventually  by  restoration  of  the  normal  cardiac  action. 

Fig.  26  and  27  were  taken  from  a  young  girl  who  had 
experienced  an  attack  of  acute  rheumatism  a  year  before. 
The  girl  sought  advice  for  pains  in  the  neck  and  chest,  and  a 
slight  irregularity  of  the  pulse  was  noticed  at  her  preliminary 
examination,  while  she  lay  quiet.  The  special  examination 
revealed  the  disordered  heart  action  which  has  been  described. 
What  was  its  significance  %  Partial  heart-block  appearing; 
in  cases  of  early  rheumatic  heart  disease  is  one  of  our  few 
reliable  signs  of  invasion  of  the  cardiac  muscle.  Chronic 
rheumatic  heart  disease,  in  its  fully  developed  form,  is  not 
made  in  a  day  ;  an  unhealthy  aortic  valve  may  suddenly 
collapse  it  is  true,  but  thickened  mitral  cusps  and  hypertrophic 
and  degenerate  muscle  take  years  to  develop.  They 
develop,  to  my  mind,  as  a  result  of  repeated  infections^ 
often  slight  and  passing  unnoticed.  It  is  along  these  lines 
that  we  may  read  the  curves  (Fig.  26  and  27)  ;  they  evidence 
a  slight  but  acute  cardiac  muscle  lesion,  a  lesion  which  is  but 
one  step  in  the  course  of  what  may  become  a  chronic  and 
incurable  malady.  The  picture  is  not  an  uncommon  oner 
and  often  it  is  combined  with  a  clear  source  of  infection  -r 
the  channel,  maybe  the  throat,  is  found  and  sealed. 

The  electrocardiogram  in  this  instance  took  us  further  \. 
while  the  patient  stood  or  gently  exercised  in  the  recumbent 
position,  the  pulse  was  regular  (Fig.  26),  and  there  was  no- 
trace  of  diastolic  murmur.  Such  was  the  condition  when 
she  was  first  seen.  When  the  pulse  was  irregular  a  murmur 
was  audible  from  time  to  time.  The  characteristic  murmur 
of    early    stenosis    of     the    mitral    orifice    was    heard    only 


Auriculo-ventricular   Heart-block,  etc.  43 

when  the  heart's  action  was  such  that  the  auricular  and 
ventricular  systoles  lay  separate.  When,  as  in  Fig.  27,  the 
contractions  were  simultaneous  and  the  auricle  forced  no 
blood  into  the  ventricle  the  murmur  vanished.  These 
electrocardiograms,  therefore,  not  only  explained  the  nature 
of  the  heart  irregularity,  its  reaction  to  posture  and  exercise, 
which  was  at  first  so  puzzling,  but  they  prompted  the  search 
for  the  characteristic  murmur  during  the  irregular  heart 
periods  ;  finally,  they  told  clearly  of  an  acute  invasion  of  the 
cardiac  muscle,  in  a  child,  up  and  about  and  otherwise 
seemingly  almost  well. 

The  curve  shown  in  Fig.  29  was  taken  from  a  case  of 
mitral  stenosis  in  which  digitalis  was  being  administered. 
This  drug  frequently  produces  heart-block  and  that  which  is 
shown  in  the  illustration  resulted  from  poisoning.  The 
electrocardiogram  demonstrated  that  the  patient  was  fully 
under  the  influence  of  the  drug. 

Complete  heart-block. 
Partial  heart-block  is  at  all  times  an  unstable  condition  ; 
it  passes  from  one  grade  to  another.  In  this  it  contrasts 
with  complete  heart-block  which  is  the  next  disorder  to  be 
considered.  We  have  seen  that  partial  heart-block  may  be 
present  while  the  ventricular  action  is  regular  (Fig.  24) 
or  irregular,  and  while  it  is  rapid  (Fig.  26)  or  slow  (end  of 
Fig.  29).  Complete  heart-block  is  generally  associated  with 
a  perfectly  regular  and  slow  ventricular  action.  The  auricles 
beat  at  their  usual  rates  and  regularly,  the  ventricles  also  beat 
rhythmically,  usually  at  a  rate  of  about  30  per  minute 
and  quite  independently  of  the  auricles.  The  electrocardio- 
graphic curves  portray  the  condition  to  perfection  and 
immediately  distinguish  it  from  all  other  forms  of  slow 
ventricular  action.  Fig.  30  is  an  example  ;  in  this  curve 
portions  of  four  ventricular  beats  are  represented  at  regular 


44 


Chapter   IV. 


Auriculo-ventricular   Heart-block,  etc.  45 

intervals  ;  each  consists  of  R,  S  and  T  deflections  of  normal 
form.  During  the  diastoles  evident  P  summits  (P1,  P2, 
P4,  P5  and  P7)  appear.  The  remaining  P  summits  fall 
with  the  ventricular  systoles.  One  (P3)  falls  after  S, 
another  (P6)  falls  upon  T.  One  (P8)  is  obscured  by  its  coinci- 
dence with  R.  They  occur  equidistantly  in  the  curve. 
Fig.  27  has  already  indicated  the  accuracy  with  which  the 
auricular  and  ventricular  electric  effects  superimpose  when 
the  systoles  are  simultaneous  ;  it  is  in  complete  heart-block 
that  this  rule,  the  constancy  of  which  will  be  again  impressed 
from  time  to  time,  is  so  strikingly  displayed.  A  number  of 
separate  curves  have  been  taken  from  the  same  patient  and 
the  separate  ventricular  complexes  have  been  isolated  and 
rearranged  one  above  the  other,  not  in  the  order  in  which 
they  occurred,  but  in  the  order  which  displays  the  summation 
most  clearly.  The  rearrangement  is  seen  in  Fig.  33.  A 
single  ventricular  and  two  auricular  complexes  are  shown 
in  each  curve  of  this  figure.  Traced  from  above  downwards, 
the  first  auricular  summits  pass  gradually  into,  through 
and  beyond  the  opening  phases  of  ventricular  systole  ;  the 
second  auricular  summits  of  the  curves  continue  the  tale, 
showing  the  passage  over  and  clear  of  the  broad  summit  T . 
In  each  instance,  where  it  occurs,  summation  is  accurate. 
The  dissociation  between  the  rhythms  of  the  two  chambers 
is  thus  paraded  in  unmistakable  garb. 

The  electric  curves  of  complete  heart-block  teach  us 
more  than  that  the  heart  is  generating  two  distinct  rhythms. 
The  slower,  or  ventricular,  rhythm  is  represented  by  curves 
of  perfectly  normal  outline  (Fig.  30).  The  contractions  are 
awakened  therefore  through  the  normal  channels.  The 
channels  which  carry  the  normal  impulses  from  auricle  to 
ventricle  also  convey  the  impulses  of  the  independent 
ventricular  rhythm.  The  impulses  are  of  supraventricular 
origin.     Yet  these  impulses  do  not  arise  in  the  auricle,  for 


46 


Chapter  IV. 


that    chamber   contracts 


Fig.    33.     A  figure  constructed 

from  the  electrocardiograms 
of  the  patient;  whose  curve 
is  shown  in  Fig.  31.  Single 
ventricular  complexes  have 
been  re-arranged  above 
each  other  so  as  to  display 
their  varying  relation  to  the 
auricular    complexes. 


under  the  influence  of  the  sino- 
auricular  node.  The  new  ventri- 
cular impulses  are  shown  to  arise 
therefore  in  the  junctional  tissues 
themselves. 

Fig.  31  is  published  to  demon- 
strate that  Q  is  a  ventricular  effect. 
The  curve  is  again  one  of  complete 
heart-block,  the  auricular  and 
ventricular  rhythms  being  inde- 
pendent ;  Q  is  constantly  asso- 
ciated with  the  ventricular  and  not 
with  the  auricular  contraction  ;  the 
same  fact  is  established  by  Fig.  28. 
In  complete  heart-block  devi- 
ations of  the  ventricular  complexes 
from  the  normal  outlines  are  to  be 
interpreted  according  to  the  usual 
rules,  as  they  apply  to  hearts  beat- 
ing with  the  normal  sequence  of 
chamber  contraction.  Fig.  32  illus- 
trates the  third  lead  in  a  case  of 
complete  dissociation  ;  the  ventri- 
cular curves  indicate  preponder- 
ance of  the  left  ventricle.  The 
same  figure  is  complicated  by  beats 
of  the  ventricle  which  occur  before 
the  anticipated  points.  They  are 
premature  beats  (P.  B.)  or  ex- 
trasystoles,  the  nature  of  which 
will  be  described  more  fully  in 
the  next  chapter.  The  auricular 
summits  are  traceable  throughout 


Auriculo-ventricular   Heart-block,  etc.  47 

the  whole  curve,  whether  they  fall  with  the  supraventricular 
or  anomalous  form  of  ventricular  curve. 

Slow  action  of  the  ventricle. 

In  partial  heart-block  when  each  second,  third  or 
iourth  auricular  systole  stimulates  the  ventricle,  and  when, 
too,  the  auricular  rate  is  normal,  the  ventricular  action  is 
necessarily  slow.  The  ventricular  action  is  also  slow,  as 
lias  been  seen,  in  complete  heart-block. 

It  is  necessary  that  slow  ventricular  rhythms  of  these 
types  should  be  clearly  distinguished  from  others  in  which 
the  heart's  action  is  different.  To  take  the  most  familiar 
examples  first,  when  the  ventricle  beats  slowly  in  jaundiced 
patients  or  in  those  who  are  convalescent  from  acute 
infections,  the  retardation  results  from  a  similar  slow  action 
of  the  auricle.  The  rhythm  of  all  chambers  is  slow,  but  the 
natural  sequence  of  chamber  beating  is  maintained.  Such 
slowing  results  from  high  vagal  tone,  for  the  heart  quickens 
in  response  to  effort  or  such  drugs  as  atropine  ;  the  quickening 
is  gradual  and  takes  several  minutes  or  more  in  its  accom- 
plishment. To  the  same  class  belongs  the  slow  heart  action 
of  many  healthy  adults.  All  these  true  bradycardias 
exhibit  an  electrocardiographic  picture  similar  to  that  shown 
in  Fig.  34  ;  each  ventricular  beat  is  preceded  by  a  single 
.auricular  beat  and  both  are  of  the  normal  type. 

But  there  is  another  and  very  special  form  of  slow  action 
which  involves  the  whole  heart  and  in  which  chamber  sequence 
is  also  undisturbed  (Fig.  34).  On  rare  occasions  patients 
Are  observed  in  whom  the  rate  of  the  ventricle  is  persistently 
maintained  at  between  30  and  40  beats  per  minute  while  they 
rest.  The  hearts  of  which  I  speak  react  in  a  curious  way  to 
exercise  ;  the  acceleration  is  not  gradual,  there  is  an  abrupt 
passage  of  slow  into  fast  rate  from  one  heart  cycle  to  the 
next.     The  curve  which  is  shown  was  taken  from  an  athlete  ; 


48  Chapter  IV. 

the  rate  of  contraction,  while  at  rest,  was  usually  36  per 
minute  ;  the  first  effect  of  exercise  was  an  abrupt  and. 
approximate  doubling  of  rate  ;  further  acceleration  was- 
gradual  ;  similar  events,  though  ordered  reversely,  were 
observed  at  the  cessation  of  effort.  This  action  of  the 
heart  will  be  spoken  of  again  in  a  later  chapter  ;  it  belongs 
to  a  series  of  phenomena  which  are  at  present  classed  under 
the  term  "  sino-auricular  block."  Sufficient  for  the  time 
being  to  state  that  it  is  infrequent,  but  that  its  confusion 
with  auriculo- ventricular  block  should  be  avoided. 

When  the  auricular  action  is  slow  and  the  ventricle  is 
starved  of  its  full  quotient  of  impulses,  the  latter  frequently 
develops  the  same  automatic  action  as  is  observed  in  com- 
plete heart-block  ;  so  that  although  there  is  no  fault  in 
conduction,  yet  two  impulse  centres,  auricular  and  ventricular 
respectively,  are  active  and  give  rise  to  responses  when 
opportunity  offers.  The  auricular  action  is  generally  the 
dominant  one,  but  if  its  rate  falls  below  a  certain  point  or 
if  the  automatic  rate  of  impulse  formation  in  the  ventricle 
rises  above  the  same  point,  then  the  last  named  chamber 
beats  spontaneously.  Generally  this  event  is  recognisable  at 
once  in  electrocardiograms  ;  an  example  is  shown  in  Fig.  35. 
In  the  first  four  cycles  of  this  figure,  the  chambers  are  beating 
sequentially  and  slowly  at  a  rate  of  50  per  minute.  The  fifth 
cycle  shows  a  ventricular  complex  of  the  usual  form,  but 
this  beat  is  not  a  response  to  an  auricular  contraction,  the 
P-R  interval  is  curtailed  and  there  is  partial  coincidence  of 
the  chamber  contractions.  This  coincidence  is  more 
pronounced  in  the  last  cycle  of  our  illustration,  where  the 
P-R  interval  is  minute.  Now  each  ventricular  complex 
is  of  normal  outline  ;  so  also  is  each  auricular  complex,  so  far 
as  it  is  visible  ;  the  ventricular  beats  are  therefore  all  of 
supraventricular  origin,  while  the  auricular  beats  are  all 
derived  from  the  natural  pacemaker.     Yet  the  ventricular 


Auriculo-ventricvlar   Heart-block,  etc. 


49 


■K 


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M: 


ii 


S  * 


§£' 


50  Chapter   IV. 

beats  are  of  two  kinds  ;   the  first  four  are  of  supraventricular 
origin  in  virtue  of  their  response  to  auricle  ;    the  last  two 
are  of  supraventricular  origin  in  virtue  of  the  impulses  formed 
in  the  junctional  tissues,  the  usual  birth  place  of   ventricular 
automatism.     When   the   ventricle   originates   a   rhythm   of 
its  own  it  is  this  centre  which  is  active  ;   the  ventricular  beats 
are  termed  "  escaped  "  ventricular  contractions  when  they 
are  isolated  or  in  short  groups.     The  bundle  is  not  the  only 
new  centre  which  may  come  into  play  when  the  natural 
pacemaker   is    sluggish  ;     other    regions    occasionally    usurp 
the  function  of  the  natural  pacemaker  and  capture  the  lead  ; 
that  centre  which  produces  impulses  most  quickly  is  always 
responsible  for  the  dominant  rhythm.     If  the  escape  of  the 
new   centre   is   continued,   the   rhythm   of  the   whole   heart 
becomes  controlled  from  that  centre  ;    that  has  happened  in 
Fig.  36.     This  figure  shows  ventricular  complexes  only  and  a 
regular  action  at  48  per  minute.     The  auricular  representa- 
tives   are    not    seen.        Such   electrocardiograms    are    found 
when  auricle  and  ventricle  contract  simultaneously  in  response 
to  impulses  created  in  the  neighbourhood  of  the  auriculo- 
ventricular  node  ;     the   mechanism  is   consecpiently  termed 
"  nodal  rhythm."     When  the  ventricle  contracts  in  response 
to  impulses  derived  from  this  centre,  its  electrical  complexes 
are  naturally  of  the  supraventricular  type.       On  the  other 
hand,  the  auricular  complexes  are  abnormal,  for  the  auricular 
contraction  wave  is  propagated  in  an  abnormal  direction. 
Having   an   abnormal  form   and   falling   at   the   same   time 
as  the  ventricular  contractions,   they  cannot   as   a  rule  be 
identified  in  the   curve,  which  therefore   shows  ventricular 
beats  only.* 

Escaped  beats  of  the   ventricle   or  auriculo-ventricular 
node     are    without    clinical    significance  ;     they    are    nearly 

*  Another  form  of  "  nodal  rhythm  "  is  shown  in  Fig.  63,  where  there  is 
a  simple  shortening  of  P-  R  interval  and  an  inversion  of  the  auricular  complex. 


Auriculo-ventricular   Heart-block,  etc.  51 

always  dependent  upon  relatively  slow  action  of  the  natural 
pacemaker,  and  it  is  to  this  that  attention  should  be  directed. 
Yet  it  is  important  that  they  should  be  recognised  when 
seen,  and  they  are  generally  clear  in  electrocardiograms. 


E  2 


(      52     ) 


Chapter  V. 


PREMATURE  CONTRACTIONS  OR  EXTRASYSTOLES. 

Premature  contractions,  or  extrasystoles,  are  responsible 
for  the  majority  of  those  pulse  disturbances  which  are 
included  in  the  term  "  intermittence."  They  are  abnormal 
contractions  of  the  heart,  which  generally  spring  from  some 
region  of  the  musculature  other  than  the  normal  pacemaker 
or  sino-auricular  node.  T  distinguish  beats  which  arise  from 
abnormal  foci  by  the  adjective  ectopic.  A  premature  beat  is 
characterised  by  appearing  before  the  natural  beat,  which 
would  continue  the  regular  rhythm  of  the  heart,  is  due. 
There  are  two  chief  classes  of  such  beats — those  which  arise 
in  the  ventricle  and  those  which  arise  in  the  auricle.  Both 
forms  are  readily  identified  in  electrocardiograms.  A  third 
type  arises  in  the  tissues  which  lie  between  auricle  and 
ventricle. 

Premature  contractions  of  ventricular  origin. 
When  the  rhythm  of  the  heart  is  disturbed  by  premature 
ventricular  contractions  (or  ventricular  extrasystoles),  the 
disturbance  of  rhythm  is  as  a  rule  limited  to  the  ventricle  ; 
the  auricle  continues  to  contract  at  the  expected  instants. 
The  premature  ventricular  beats  are  easily  recognised.  The 
electric  complexes  which  represent  them  are  known  to  be 
ventricular,  because  they  are  of  the  same  duration  as  the 
normal  ventricular  complexes  in  the  same  subject  ;  but  they 
antecede  and  usually  replace  the  regular  responses  of  the 
ventricle,    thereby   disturbing    the    rhythmic    action  ;     their 


Premature   Contractions  or   Extra-systoles. 


53 


wmmammmamm 

Fig.  37.  An  electrocardiogram  showing  two  premature  contractions,  arising  in 
the  right  ventricle.  The  curve  shows  two  buried  auricular  complexes 
of  normal  outline.  These  premature  contractions  are  responsible  for  the 
commonest  forms  of.  intermittent  pulse  (see  Fig.  27). 


Fig. 


minnuuuJ 


38.  Premature  contractions  arising  in  the  ventricle,  replacing  the 
alternate  normal  ventricular  beats  and  giving  rise  to  one  form  of  bigeminy 
of  the  ventricle  and  pulse.  The  figure  illustrates  the  manner  in  which 
buried  auricular  complexes  may  be  identified. 


tmrnmnTEi 


Fig.  39.  Two  premature  contractions  arising  in  the  right  ventricle.  They 
occur  together  and  replace  a  single  normal  ventricular  contraction.  The 
rhythmic  auricular  contraction  falls  with  the  first  premature  beat 


Fig.   40.     Bigeminy  of  the  ventricle,  resulting  from  premature  contractions 
of  the  ventricle.     The  premature  beats  arise  from  two  separate  foci. 


54  Chapter  V. 

form  is  anomalous.  These  points  are  illustrated  by  Fig.  37. 
The  figure  commences  with  a  perfectly  normal  heart  cycle 
(P,  R  and  T)  ;  this  is  followed  by  a  tall  and  pointed  summit 
(P.  B.),  which  in  turn  is  followed  by  a  broad  downward 
deflection.  The  total  length  of  this  anomalous  complex  is 
equal  to  that  of  R  and  T  in  the  normal  cycles.  Succeeding 
the  disturbance  are  three  regular  cycles  and  the  disturbance 
is  repeated.  Now  the  premature  beats  of  this  figure  are 
spontaneous  and  arise  in  the  ventricle,  for  no  auricular 
contractions  precede  them  ;  they  are  ectopic  in  origin.  The 
auricular  rhythm  is  undisturbed  ;  the  distance  between 
P1  and  P3  is  exactly  equal  to  the  distance  between  P3  and 
P5.  Where  then  is  P2  ?  It  lies  embedded  in  the  complex 
of  the  premature  beat.  That  this  is  so  is  ascertained  by 
comparing  the  two  premature  beats  of  the  figure  ;  when  the 
second  occurs,  the  auricular  rate  has  become  a  little  slower 
and  consequently  the  buried  auricular  complex  (P6)  lies  a 
little  more  to  the  right,  relative  to  the  corresponding  prema- 
ture beat,  than  does  P2.  The  two  premature  beats  give 
complexes  of  exactly  the  same  form,  the  only  difference 
between  the  two  curves  is  engendered  by  the  auricular 
complexes  which  fall  with  them  ;  this  difference  is  slight, 
and  is  due  to  the  time  relations  of  the  several  events.  The 
buried  auricular  beats  being  recognised,  the  curve  as  a  whole 
may  be  analysed  fully.  The  auricular  systoles  are  represented 
throughout  ;  they  occur  in  regular  sequence.  After  each 
premature  beat,  the  ventricle  is  silent  ;  it  is  waiting  for 
the  next  auricular  impulse,  to  which  it  will  respond.  The 
long  diastole  which  thus  compensates  for  the  prematurity  of 
the  abnormal  ventricular  contraction  is  spoken  of  as  the 
"  compensatory  pause."  AH  the  auricular  complexes  of  this 
figure  are  of  normal  type,  for  all  have  arisen  at  the  pace- 
maker ;  all  but  two  of  the  ventricular  complexes  are  of  normal 
type,   for  they  have  originated   in  impulses   traversing   the 


Premature   Contractions  or  Extr asystoles. 


55 


normal    paths.     Two    of    the    ventricular    complexes    are 
anomalous    in    outline,     showing    that    the    corresponding 


^ 


EB. 


i.i  ii  tniiiiiiu 


■ininiimr"! ' J 


unTminiiiiuummmimm^tfipjfjfy 


Fig.  41  and  42.  Figures  illustrating  the  two  chief  types  of  premature 
contractions  of  ventricular  origin  as  they  are  portrayed  in  the  separate 
leads.  Fig.  4l  shows  a  premature  beat  which  arises  in  the  right  ventricle  ; 
Fig.  42  shows  a  premature  beat  arising  in  the  left  ventricle. 

excitation  waves  have  run  abnormal  courses  ;  the  course  has 
been  abnormal  because  the  starting  point  of  the  wave  has 
been  abnormal. 


56  Chapter   V. 

Premature  ventricular  contractions  in  different  subjects 
yield  electric  curves  of  very  different  forms  independently 
of  the  lead  from  which  the  curves  are  derived.  The  pictures 
are  also  different  in  different  leads  in  the  same  individual. 
In  interpreting  the  curves,  therefore,  they  may  not  be  treated 
pictorially,  each  should  be  analysed  in  detail  and  upon  the 
general  lines  which  I  have  tried  to  summarise.  Another 
curve  is  shown  (rig.  38)  which  illustrates  the  manner  in 
which  buried  auricular  contractions  are  discovered.  The 
premature  beats  show  two  main  deflections,  one  pointed 
and  directed  down  and  the  other  rounded  and  directed  up. 
The  shoulder  of  the  rounded  upstroke  is  modified  by  a  super- 
imposed auricular  representative  (P)  in  each  case,  but  it  falls 
at  slightly  different  points  relative  to  the  two  premature 
beats.  Two  successive  premature  beats  are  shown  in  Fig.  39. 
They  take  the  place  of  a  single  normal  ventricular  contraction. 
The  single  rhythmic  auricular  complex,  which  is  buried,  falls 
upon  the  downstroke  of  the  first  premature  beat.  If  the 
two  beats  are  compared,  they  will  be  found  to  differ  chiefly 
in  this  respect.  Premature  beats  from  separate  ventricular 
foci  are  shown  in  Fig.  40.  Two  are  of  the  same  form  as  those 
of  Fig.  37  ;  the  third  or  central  one  consists  of  three 
deflections,  a  short  spike,  a  deep  and  pointed  depression 
and  a  rounded  summit.  The  auricular  contraction,  which  falls 
between  the  last  two,  is  prominent  and  unmistakable. 

There  are  two  chief  types  of  premature  contractions  of 
ventricular  origin  ;  one  comes  from  the  right  ventricle 
(Fig.  41)  ;  the  other  comes  from  the  left  ventricle  (Fig.  42  ; 
see  Fig.  45  also).  In  any  given  case  the  shape  of  the  electrical 
curves  is  usually  very  similar  in  leads  II  and  ///,  but  as  a 
rule  the  direction  of  the  deflections  is  reversed  in  lead  / 
(Fig.  41),  though  this  is  not  invariably  the  case  (Fig.  42). 
The  complexes  of  extrasystoles  arising  in  the  ventricles  are 
not   dissimilar  to   those   seen  in  the  lesions   of  the   bundle 


Premature   Contractions  or  Extrasy  stoles. 


57 


3Z1 


P.B. 


.iiil.iiiiiiiiiiiiiiiimiiiimiiiiin.niiiiiiiiiiniiiiMnimiiniiiiiiiniiiii'iiimiMiniiiiiiiii'niiH.m 

Fig.   43.     Premature  contractions  arising  in  the  right  ventricle  and  interpolated 
between  normal  heart  cycles. 


Pig.  44.     Interpolated  premature  contractions  of  ventricular  origin. 


f — r — 

,  1      JK~ 

"i^"'~i — ' 

— z- 

—/— v — 

^.^T^wy  ?n/~W<V  jj\tat   ' — *"WV  ff  ^f^J  /**  ^K^t  <#mMPl 

" 1 

-h — ; — 

— tr 

^^^ 

=-^ '- 

1 

— $&=- 

o 

j 

Fig.   45.     Premature  contraction  arising  in  the  left  ventricle. 


Fig.  46.  Premature  contractions  arising  in  the  ventricle,  late  in  diastole. 
The  auricular  systole  has  begun,  and  in  one  instance  is  almost  complete, 
before  the  extras ystole  of  the  ventricle  begins. 


Z^ttmZ^Jr'fi  T7ZE£^f&. 


Fig.  47.  Prom  the  same  patient  as  Fig.  46,  showing  interference  between 
two  waves  of  contraction  in  the  ventricle  (see  text).  A  premature 
contraction  of  auricular  origin  is  seen  towards  the  end  of  this  figure. 


58  Chapter  V. 

divisions.  In  experiment  stimulation  of  the  right  ventricle- 
(Fig.  15  at  A)  yields  curves  similar  to  a  lesion  of  the  bundle 
branch  at  A1  ;  that  is  natural  since  in  both  instances  the  wave 
is  propagated  from  the  same  region  of  the  heart.  Similarly,, 
stimulation  of  the  left  ventricle  (Fig.  15,  at  B)  yields  curves- 
which  resemble  those  following  a  lesion  of  the  bundle  branch. 
at  B1. 

Although  premature  contractions  of  ventricular  origin 
are  generally  followed  by  "  compensatory  pauses,"  this  only 
happens  when  the  rhythmic  auricular  impulse  finds  the- 
ventricle  already  in  contraction.  The  ventricle  is  then 
"  refractory  "  to  stimulation.  This  is  the  reason  why  there 
is  no  response  to  buried  auricular  contractions,  such  as- 
are  seen  in  Fig.  37  and  38.  But  if  the  heart  is  beating; 
slowly  and  the  extrasystolic  beats  of  the  ventricle  are  very 
premature,  the  extra  ventricular  beat  may  have  terminated 
before  the  next  auricular  impulse  arrives.  In  such  circum- 
stances the  premature  beat  does  not  replace  a  normal 
ventricular  event  (Fig.  43  and  44)  but  is  an  added  pheno- 
menon.    Such  beats  are  called  "  interpolated  extrasystoles." 

When  a  premature  contraction  falls  very  late  in  diastole, 
the  disturbance  of  ventricular  rhythm  is  slight,  for  it  happens 
at  an  instant  close  to  that  at  which  a  rhythmic  beat  is  expected. 
The  auricle  may  even  contract  before  the  premature  beat 
of  the  ventricle  begins,  in  which  case  there  is  an  appreciable 
though  shortened  interval  between  the  auricular  beat  and 
the  premature  one.  The  origin  of  the  latter  is  nevertheless 
clearly  shown  by  the  shape  of  its  electric  complex.  An 
example  of  this  phenomenon  is  seen  in  Fig.  46.  But 
supposing  that  the  premature  beat  comes  so  late  that  an 
auricular  impulse  is  already  well  on  its  way  to  the  ventricle, 
then  two  waves  of  contraction,  one  propagated  from  the 
normal  source  and  the  other  propagated  from  the  source  of 
irritation  in  the  ventricle,  may  travel  over  that  chamber  and 


Premature   Contractions  or  Extrasy stoles.  59 

meet  somewhere  in  its  walls.  In  such  circumstances  the 
electric  complex  of  the  ventricular  contraction  will  be  of 
transitional  form.  Fig.  46  and  47  were  taken  from  the  same 
patient.  The  usual  form  of  anomalous  beats  is  seen  in  Fig.  46. 
Each  of  the  three  premature  contractions  of  this  figure 
produce  similar  electric  curves  ;  each  falls  late  and  after  the 
auricular  contraction  has  started.  The  first  premature  beat 
of  Fig.  47  comes  still  later  in  diastole  ;  the  interval  between  it 
and  the  preceding  auricular  beat  is  only  just  perceptibly  less 
than  the  normal  P-R  interval.  The  resultant  ventricular 
curve  has  a  distinct  form,  in  which  traces  of  the  normal  and 
traces  of  the  abnormal  electric  curves  are  seen.  Such  a 
contraction  results  when  simultaneous  but  independent 
excitation  waves  meet  in  the  ventricular  walls. 

Premature  contractions  of  auricular  origin. 
When  a  new  impulse  is  born  in  the  auricle,  the  dis- 
turbance is  never  confined  to  this  chamber.  The  premature 
auricular  contraction  awakens  a  response  in  the  ventricle. 
A  simple  example  of  the  auricular  extrasystole  is  shown  in 
Fig.  48.  The  first  and  second  cycles  of  the  figure  are  normal, 
consisting  of  P,  Q,  R,  S  and  T  deflections.  The  third  cycle 
is  premature.  Consider  first  the  ventricular  complex  of 
this  premature  beat.  It  has  a  perfectly  normal  outline.  The 
impulse  responsible  for  it  is  known  therefore  to  have  travelled 
along  the  normal  channels  ;  that  is  to  say,  it  has  come  down 
through  the  auriculo- ventricular  bundle  and  its  branches. 
It  is  a  ventricular  beat  of  supraventricular  type  (see  page  24). 
When  we  search  for  the  cause  of  this  ventricular  beat,  we  find 
it  in  an  auricular  contraction  which  has  just  been  completed. 
But  this  auricular  beat  is  of  abnormal  type,  the  electric 
curve  shows  a  depression  and  not  a  summit.  To  what  is  the 
inversion  due  ?  It  is  the  result  of  the  abnormal  path  which 
the  excitation  wave  has  taken  in  the  auricle.     The  impulse, 


60 


Chapter   V. 


from  which  the  whole  premature  heart  cycle  results,  has 
been  generated  in  an  abnormal  auricular  focus,  i.e.,  in  a 
region  lying  at  a  distance  from  the  pacemaker.  It  has  arisen 
from  an  ectopic  centre  and  the  wave  has  consequently  passed 
through  the  auricle  in  a  direction  other  than  normal  ;    but 


tiiTTniiniiinimiinTiirrniiiiiitTTiiitmiimmTnTimrnnnmiiiiinTrmttTnn;iii),iiiiniiiiHiiiiiTiinT.iiiii  i  miuu  l.miHnJB 


Fig.  48.  A  single  premature  contraction  of  auricular  origin.  The  auricular 
complex  is  alone  abnormal. 

Fig.  49.  Three  isolated  premature  contractions,  arising  in  the  auricle. 
The  corresponding  auricular  complexes  are  abnormal,  and  there  is  also 
slight  distortion  of  the  corresponding  ventricular  complexes  (aberration). 

Fig.  50.  A  single  premature  contraction,  probably  arising  in  the  immediate 
neighbourhood  of  the  sino-a,uricular  node. 


having  arisen  in  the  auricle,  it  travels  to  the  ventricle  along 
the  only  path  open  to  it,  namely,  that  constituted  by  the 
normal  channels.  Usually,  the  diastole  which  follows  a 
premature  auricular  contraction  is  not  compensatory  ;  it  is 
too  short,  and  consequently  the  fundamental  rhythm  of  the 


Premature   Contractions  or   ExtrasystoJ.es. 


61 


heart  is  disturbed.  A  rare  example  of  premature  auricular 
contractions,  in  which  this  diastole  is  almost,  if  not  cpiite. 
compensatory,  is  shown  in  Fig.  49.  The  auricular  complexes 
are  inverted  in  this  figure,  as  they  are  in  Fig.  48.     When  a 


- 


-JL:- 


rfi- 


~^f 


-ff  ! 


&zl 


P±p5 


Fig.  51.  A  tingle  premature  contraction  of  auricular  origin.  The  first 
beat  after  the  pause  originates  in  the  same  point  as  the  premature  one. 

Fig.  52.  Two  isolated  premature  contractions  of  auricular  origin.  The 
premature  auricular  systole  coincides  with  the  preceding  ventricular 
contraction  ;  P  and  T  are  thus  superimposed.  Taken  from  a  case  of 
mitral  stenosis. 

Fig.  53.  Three  successive  premature  contractions  of  auricular  origin.  Taken 
from  a  case  of  mitral  stenosis  ;  note  the  split  P  summits  in  this  and  the 
preceding  figure. 

premature  beat  arises  in  or  near  the  sino-auricular  node,  then 
the  whole  premature  electric  curve  is  of  normal  form,  as 
shown  in  Fig.  50;  the  P  summits  are  similar  throughout, 
showing   the   similar   origins   of   the   beats  ;     moreover,   the 


62  Chapter   V. 

diastole  which  follows  the  premature  beat  is  unduly  shortened  ; 
its  length  is  either  the  same  or  somewhat  shorter  than  that 
of  the  usual  rhythmic  beats. 

On  all  but  rare  occasions  the  beats  which  follow  a 
premature  contraction  are  derived  from  the  pacemaker  ;  the 
old  heart  rhythm  is  immediately  restored  (Fig.  48)  ;  but  it 
sometimes  happens  that  the  first  beat  of  the  returning  rhythm 
is  also  ectopic  (Fig.  51)  and  springs  from  the  same  centre  as 
the  extrasystole.  A  not  dissimilar  disturbance,  but  of  higher 
grade,  is  shown  in  Fig.  63. 

When  new  impulses  are  created  in  the  auricle,  the 
premature  auricular  contraction  may  fall  so  early  as  to 
coincide  with  the  preceding  ventricular  systole.  P  and  T 
then  fall  together  and  summate.  Summation  of  these 
summits  is  seen  in  Fig.  49  and  50,  but  is  clearer  in  Fig.  52, 
where  P  and  T  are  both  prominent.  The  second  and 
fourth  beats  of  the  last  named  figure  are  premature  and 
arise  at  an  ectopic  auricular  focus.  The  P  summit  of  the 
premature  beat  coincides  with  the  T  summit  of  the  preceding 
cycle  and  combines  with  it  to  form  a  tall  blunt  summit. 
Simple  superimposition  of  P  and  T  would  not  yield  a  united 
summit  of  the  type  depicted,  for  the  rhythmic  P  is  bifid 
in  this  case  ;  it  is  known,  therefore,  that  the  premature  beats 
were  ectopic  in  origin. 

An  example  of  premature  auricular  contractions,  occurring 
in  succession,  is  shown  in  Fig.  53.  Each  premature  auricular 
complex  coincides  with  a  preceding  T  summit.  All  told, 
there  are  three  of  them. 

While  it  is  the  general  rule  that  the  ventricular  complex 
of  a  premature  auricular  contraction  is  of  normal  outline, 
yet  its  form  often  diverges  ;  it  may  diverge  so  conspicuously 
as  to  be  mistaken  for  a  beat  of  ventricular  origin.  The 
premature  R  summits  of  Fig.  49  and  52  are  taller  than  those 
of  rhythmic  beats  ;   but  the  difference  in  general  outline  is  but 


Premature   Contractions  or  Extra-systoles. 


63 


slight.  Examples  of  the  chief  forms  of  conspicuous  divergence 
-are  illustrated  in  Fig.  54,  which  consists  of  four  strips  of  curve 
taken  from  the  same  patient.  In  the  first  curve  is  a 
premature  auricular  contraction  which  conforms  to  the  general 
rule  ;7all  the  ventricular  complexes  of  this  strip  are  similar  ; 


"  " 


rZ- 


IFig.  54.  Four  curves  from  a.  single  subject.  Each  shows  a  solitary  premature 
auricular  contraction.  The  premature  auricular  complex  falls  with  the 
commencement  of  the  preceding  T  and  notches  it.  The  corresponding 
ventricular  complexes  of  the  first  three  curves  are  of  various  format 
the  central  curves  illustrate  a  phenomenon  which  is  described  under  the 
term  '-aberration. "  In  the  last  curve  the  premature  auricular  contraction 
is  blocked. 


the  premature  beat  (the  third  in  the  curve)  is  evidently  of 
supraventricular  origin.  The  abnormal  auricular  complex 
notches  the  upstroke  of  the  preceding  T  summit  ;  this  is 
■appreciated  when  T1  and  T2  are  compared  ;    they  have  not 


64  Chapter   V. 

the  same  shape,  and  the  difference  is  due  to  an  inverted  P 
falling  with  T2.  The  second  and  third  curves  show  precisely 
similar  events,  Tz  is  notched  by  an  abnormal  auricular 
representative  in  both  instances  ;  but  in  these  curves  the 
premature  auricular  contractions  give  rise  to  ventricular  beats 
of  anomalous  type.  In  the  second  curve  the  complex  consists 
of  two  upwardly  directed  summits,  the  first  of  which  is  bifid  ■ 
in  the  third  curve  upward  and  downward  deflections  of  equaL 
extent  are  followed  by  a  rounded  summit.  Both  the  curious 
beats  were  of  supraventricular  origin,  for  each  followed  an 
auricular  systole  which  is  to  be  detected  in  the  curve  ;  the 
abnormality  of  the  ventricular  curves  is  attributed  to 
deficient  conduction  along  certain  tracts  of  the  junctional 
tissues,  whereby  the  auricular  impulse  has  pursued  an 
abnormal  course  to  the  ventricle  ;  the  deficiency  has  been 
confined  to  the  premature  beats  because  the  rest  preceding^ 
these  has  been  brief.     The  electric  curves  exemplify  aberration 

-fi-     R   :R  *  -    r    1 


-•FJ^-"-->t  ■'   \PT    :    P.  T  fLTlPZ 


i/20  S  S     s  S         $ 

Fig.   55.     Two  premature  contractions  arising  in  the  junctional  tissues. 

(see  page  27).  Auricular  extrasystoles,  showing  aberrant- 
ventricular  complexes,  are  almost  confined  to  hearts  in  which 
conduction  defects  are  demonstrable.  The  conduction 
intervals  of  the  premature  beats  are  prolonged  in  the  second 
and  third  curves  of  the  present  figure  ;  and  in  the  fourth  or 
last  curve  a  premature  auricular  contraction  is  blocked  ;  Tz 
is  again  notched  by  an  inverted  P,  but  the  auricular  systole 
which  the  latter  represents  is  not  followed,  as  in  the  other 
curves,  by  a  response  of  the  ventricle. 


Premature   Contractions  or  Extrasy stoles.  65 

Premature  contractions  arising  in  the  junctional  tissues. 

Although  the  majority  of  premature  contractions  arise 
in  the  auricle  or  in  the  ventricle,  on  occasion  the  conducting 
tissues,  which  unite  these  two  chambers,  appear  to  originate 
the  disturbance. 

There  are  two  premature  ventricular  systoles  in  Fig.  55  ; 
and  the  true  relations  of  the  auricular  and  ventricular 
contractions  in  this  figure  are  precisely  the  same  as  those  seen 
when  the  premature  beats  are  of  ventricular  origin.  The 
pauses  are  compensatory,  and  there  is  no  disturbance  of  the 
auricular  rhythm.  The  auricular  contractions  fall  regularly 
throughout  the  curve  ;  each  is  represented  by  a  normal  P 
summit,  though  two  of  these  summits  are  buried.  The 
undisturbed  auricular  rhythm  demonstrates  that  the  pre- 
mature beats  have  arisen  below  the  auricle.  Yet  they  have 
had  their  origin  above  the  main  division  of  the  auriculo- 
ventricular  bundle,  for  the  ventricular  complexes  have 
physiological  outlines  ;  the  impulses  have  been  supraventri- 
cular. The  focus  of  disturbance,  in  such  cases,  is  located  in 
the  auriculo-ventricular  node  or  in  the  main  stem  of  the 
bundle. 

Premature  contractions,  whatever  their  form,  are  always 
easy  to  recognise  in  electrocardiograms  ;  in  other  graphic 
records  they  often  produce  confusing  pictures,  and  this  is 
frequently  the  case  when  they  appear  in  groups.  The 
characters  of  the  pulse  may  closely  resemble  those  which 
are  associated  with  grave  disturbances  such  as  auricular 
fibrillation,  nutter  and  alternation.  Premature  contractions 
are  relatively  benign,  and  as  electrocardiography  may  be 
the  only  certain  method  of  differentiating  this  irregularity 
from  more  serious  disturbances,  it  is  to  be  recommended 
as  a  final  means  to  decide  where  there  is  doubt. 


(     66     ) 


Chapter    VI. 


SIMPLE    PAROXYSMAL    TACHYCARDIA. 

Electrocardiography  has  explained  many  of  the 
phenomena  of  paroxysmal  tachycardia.  In  the  first  place 
it  has  shown  that  these  transient  attacks  of  cardiac  accelera- 
tion are  not  the  result  of  simple  disturbances  of  innervation 
as  was  at  one  time  thought.  If  a  heart  accelerates  in 
response   to   exercise,   emotion,   fever   or   other   such   cause, 


Fig.  56.  An  electrocardiogram  from  a  case  of  exophthalmic  goitre.  The 
heart  rate  shown  is  150  per  minute.  The  curve  indicates  a  simple 
acceleration  of  the  normal  rhythm. 


then  the  electrocardiogram  has  in  general  a  physiological  out- 
line. Auricular  and  ventricular  complexes  retain  their  shapes, 
except  for  minor  modifications  which  are  the  simple  result 
of  the  increased  heart  rate.  Fig.  56  was  taken  from  a 
case  of  exophthalmic  goitre,  the  ventricular  rate  being 
150  per  minute.  The  curve  shows  P,  R  and  T  summits  ; 
and  these  conform  to  the  type  of  heart  beat  propagated  from 
the  natural  pacemaker. 

The    curves   of  paroxysmal   tachycardia   are   different  ; 
they  show  that  the  dominant  centre  of  impulse  formation  has 


Simple  Paroxysmal   Tachycardia. 


67 


moved  during  the  attack,  usually  to  some  other  part  of 
the  auricle.  Fig.  57  and  58  are  from  a  case  of  paroxysmal 
tachycardia  ;  each  figure  shows  the  three  leads.  The 
first  (Fig.  57)  was  taken  while  the  heart  action  was  natural, 
its  rate  being  81  per  minute.  The  shapes  of  the  auricular 
and  ventricular  complexes  in  these  curves  should  be  noticed 
and  compared  with  those  of  Fig.  58,  which  depicts  a  paroxysm 
in  which  the  heart  rate  was  146  per  minute.  It  is  seen  that 
the  ventricular  complexes  of  the  paroxysm  retain  their 
form    and    that    they    do    so    faithfully.     Each    ventricular 


Fig.  57  and  58.  Two  sets  of  curves  from  a  case  of  simple  paroxysmal  tachy- 
cardia. Figure  57  was  taken  while  the  heart  beat  slowly  ;  Fig.  58  while 
it  beat  rapidly.  The  curves  demonstrate  the  supraventricular  origin 
of  the  paroxysm.  The  inversion  of  P  in  leads  II  and  III  of  Fig.  58 
indicates  that  it  arose  in  an  ectopic  auricular  focus. 


summit  or  depression  of  Fig.  57  is  repeated  in  Fig.  58.  The 
similarity  extends  even  to  the  minutiae  of  the  curves,  even  to 
the  notch  on  the  downstroke  of  R  in  lead  //  and  the  notch  on 
the  upstroke  of  S  in  lead  ///.  The  ventricular  beats  during 
the  paroxysm  were  therefore  of  the  same  kind  as  those  of  the 
slow  period  ;  in  both  phases  the  impulses  pursued  the  same 
course  ;   that  is  to  say,  they  travelled  along  the  normal  paths 

F    2 


68  Chapter   VI. 

of  the  junctional  tissues.  The  paroxysm  was  therefore  of 
supraventricular  origin.  But  when  we  examine  the  auricular 
complexes  in  the  two  sets  of  curves,  it  is  seen  that  while  the 
P  summits  of  the  slow  period  are  upright,  those  of  the 
paroxysmal  period,  are  inverted  in  leads  //  and  ///  and  are 
also  different  in  lead  /.  These  changes  are  significant,  for 
they  tell  us  that  when  the  paroxysm  comes,  the  natural 
pacemaker  is  no  longer  the  dominant  impulse  centre,  but 
that  some  new  auricular  focus  has  an  enhanced  activity 
and  that  the  old  centre  is  outpaced.  Not  infrequently 
such  a  conclusion  as  to  the  nature  of  the  paroxysm  can 
be  maintained  from  its  intrinsic  beats  alone.  Yet  it  is 
always  more  justified  when  the  curves  of  the  two  distinct 
phases  of  heart  action  can  be  taken,  and  when  the 
similarities  and  dissimilarities  which  have  been  named  are 
-observed. 

The  similar  nature  of  paroxysms  of  tachycardia  and 
solitary  premature  beats  is  at  once  suggested  when  it  is 
observed  that  the  abnormal  beats  are  of  ectopic  origin.  There 
is  in  fact  no  essential  difference  between  the  individual  beats 
of  the  one  and  the  other.  Premature  beats  are  not  always 
solitary  ;  they  sometimes  occur  in  short  groups  (Fig.  39  and 
53)  ;  it  is  entirely  a  question  of  the  length  of  these  groups 
and  the  nature  of  our  terminology  as  to  whether  we  term  such 
small  groups  successive  premature  beats  or  short  paroxysms 
of  tachycardia.  In  one  and  the  same  case,  isolated  beats, 
short  groups  and  longer  paroxysms  may  be  found,  and  the 
electric  curves  usually  show  that  all  originate  in  the  same 
focus  (Fig.  59).  Premature  beats  are  characterised  by  the 
relatively  short  diastoles  which  precede  them  ;  rapid  impulse 
formation  is  expressed  in  the  paroxysmal  curves  by  the 
rate  of  the  heart  beat  and  by  the  prematurity  of  the  first 
paroxysmal  beat.  That  the  two  phenomena  are  essentially 
the   same   is    also    demonstrated   by   the    manner  in   which 


Simple  Paroxysmal   Tachycardia. 


69 


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70 


Chapter  VI. 


each    terminates.       The    solitary    premature    beat    and    the 
paroxysm  are  succeeded  by  a  pause  which  in  a   single  case 

is  of  constant  length,  and  there 
is  an  immediate  return  of  the 
normal  rhythm  (Fig.  59).  The 
change  from  one  rhythm  to  the 
other  in  paroxysmal  tachy- 
cardia is  absolutely  abrupt  and 
in  this  way  contrasts  with  the 
gradual  slowing  of  a  simple 
cardiac  acceleration.  Fig.  59, 
61  and  62  are  examples  of 
curves  which  show  the  offsets 
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heart  action  they  are  larger  and 

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Simple  Paroxysmal   Tachycardia.  71 

first  premature  beat  has  a  ventricular  complex  of  aberrant 
type  (see  Fig.  54,  second  curve,  and  explanation).  The 
diastole  following  the  two  premature  beats  has  the  same  length 
as  the  diastole  following  the  paroxysm.  Then  come  two 
normal  cycles  and,  after  the  last,  two  premature  auricular 
contractions  again  occur.  The  figure  clearly  shows  those 
associations  between  paroxysmal  and  premature  beats  which 
have  been  discussed. 

In  Fig.  60  and  61  are  two  curves  from  one  case.  The 
first  exhibits  a  normal  rhythm  disturbed  by  two  premature 
auricular  beats.  The  P  summits  which  are  premature  are 
smaller  than  those  of  the  rhythmic  cycles.  The  second 
shows  a  paroxysm  of  tachycardia  in  the  same  patient  ;  the 
ventricular  complexes  are  unaltered  but  the  auricular  ones 
are  inverted.  The  second  and  last  cycles  of  this  paroxysm 
are  premature,  and  are  derived  from  the  same  source  as 
those  which  are  shown  to  disturb  the  normal  rhythm  in 
Fig.  60.  A  longer  diastole  terminates  the  paroxysm  and  the 
first  beat  of  the  returning  normal  rhythm  is  shown.  Thus,  in 
this  patient,  paroxysms  of  tachycardia,  thrown  in  from  an 
ectopic  focus,  disturb  the  normal  rhythm  ;  and  both  the 
paroxysms  and  the  normal  rhythm  are  interrupted  by  single 
premature  contractions  from  a  second  ectopic  focus. 

Fig.  62  exhibits  an  electrocardiogram  and  radial  pulse 
curve  covering  the  end  of  a  paroxysm  of  tachycardia  and  the 
beginning  of  the  slow  rhythm.  The  long  post-paroxysmal 
diastole  is  well  displayed  and  there  is  a  little  quickening  of  the 
heart  rate  at  the  beginning  of  the  slow  rhythm,  a  not  unusual 
phenomenon.  If  the  ventricular  complexes  of  the  slow  and 
fast  periods  are  compared,  they  will  be  found  to  be  alike, 
except  that  at  its  commencement  T  goes  deeper  during  the 
paroxysmal  stage.  This  change  in  the  shape  of  T,  which  is 
semi-inverted  while  the  heart  rate  is  fast,  is  not  incompatible 
with   acceleration   alone.     Had   we   simply  the   paroxysmal 


72  Chapter  VI. 

curves,  or  even  the  curves  of  the  slow  and  fast  periods  for 
comparison,  then  a  complete  analysis  of  the  paroxysmal 
mechanism  would  not  be  feasible.  The  record  of  the  transi- 
tion from  one  form  of  heart  action  to  the  other  provides  us 
with  the  full  data.  If  the  last  two  cycles  of  the  paroxysm 
are  compared,  it  will  be  clear  that  T  alters  its  shape  ;  the 
semi-inversion  is  not  present  in  the  last  paroxysmal  cycle  ; 
it  is  due,  in  the  other  paroxysmal  beats,  to  the  superimposition 
of  an  inverted  P  upon  T.  The  paroxysm  has  had  its  origin 
in  a  new  auricular  focus  and  each  auricular  systole  has 
propagated  a  ventricular  systole  ;  the  rate  is  fast  (128  per 
minute)  and  the  P-R  interval  is  long  (0*33  second)  ;  so  each 
auricular  contraction  falls  with  the  preceding  ventricular 
contraction.  The  last  ventricular  beat  is  necessarily  un- 
complicated in  this  respect,  for  the  auricular  paroxysm  has 
terminated  before  the  ventricle  responds  to  the  last 
paroxysmal  impulse.  The  paroxysm  ends  in  the  usual  long 
diastole  and  the  natural  pacemaker  re-establishes  its  control  ; 
but  the  prolongation  of  the  P-R  interval  is  maintained. 

These  illustrations  show  how  valuable  is  a  comparison 
of  fast  and  slow  periods  in  electrocardiograms.  The  curves 
of  the  paroxysmal  phase  are  but  rarely  sufficient  to  provide 
a  full  analysis.  The  curves  of  both  rapid  and  slow  heart 
action  are  also  insufficient  at  times  ;  the  curves  which  show 
the  transition  from  fast  to  slow  or  from  slow  to  fast  are  the 
most  illuminating  of  all. 

Paroxysms  of  tachycardia  may  also  arise  in  one  or  other 
ventricle  ;  under  these  circumstances  the  electric  curves  of 
individual  beats  are  of  the  forms  seen  in  Fig.  41  and  42.  But 
tachycardia  of  ventricular  origin  is  comparatively  rare  in 
records.  An  auricular  origin  is  the  general  rule.  It  is 
probably  because  the  ventricular  disturbances  are  less 
compatible  with  life  that  they  are  so  rarely  recorded. 
Similar  attacks  may  also  originate  in  the  junctional  tissues, 


Simple  Paroxysmal   Tachycardia. 


73 


T)ut  the  resultant  curves  are  often  obscure  and  difficult  fully 
Where,  as  in  Fig.  61,  the  P-R  interval  is 
„,  ,  jj  slightly  reduced    and  P  is  inverted, 

it  is  customary  to  locate  the  origin 
of  the  paroxysm  in  the  upper  part 
of  the  A-V  node.  In  other  instances 
of  nodal  paroxysms,  P  and  R  fall 
together  and  the  former  cannot 
then  be  deciphered. 

The  chief  value  of  electro- 
cardiographic records  in  tachycardia 
is  in  distinguishing  between  simple 
acceleration,  simple  paroxysmal 
tachycardia  and  a  third  condition 
which  is  described  in  the  next 
chapter.  The  natural  history  of 
the  three  conditions  and  their  re- 
actions to  treatment  are  essentially 
different.  Rapid  heart  action  of 
obscure  origin  is  frequent  ;  the 
electric  method  singles  out  those 
which  are  primarily  of  cardiac 
origin  and  distinguishes  them  from 
simple  disturbances  of  innervation. 


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Dislocation  of  the  pacemaker. 

It  may  be  profitable  to  con- 
trast simple  paroxysmal  tachycardia 
with  the  disturbance  of  the  heart's 
action  which  is  shown  in  Fig.  63. 
This  electrocardiogram  opens  with 
three  cycles  inwhich  the  heart  beats 
have  been  propagated  from  the 
natural  pacemaker,  as  is  evidenced 
by    the    shape    of    the    complexes 


74  Chapter  VI. 

(S  is  deep  because  the  curve  was  taken  from  a  patient  in. 
whom  there  was  a  preponderance  of  the  left  ventricle  ; 
the  curve  is  from  lead  ///).  The  fourth  beat  is  a  pre- 
mature contraction  of  auricular  origin.  The  usual  pause 
succeeds  this  disturbance,  and  subsequently  rhythmic  heart 
action  is  resumed.  But  the  restored  rhythm  arises  from 
a  i  new  focus,  as  is  shown  by  the  shape  of  the  auricular 
complexes.  There  is  little  or  no  difference  in  the  rate  of  the 
heart  before  and  after  the  disturbance,  and  in  this  respect 
the  curve  contrasts  with  those  of  paroxysmal  tachycardia. 
The  ectopic  rhythm  is  developed  in  this  instance  from  the 
same  type  of  impulses  as  is  the  normal  rhythm  ;  unlike  the 
paroxysms  of  rapid  heart  action,  it  is  not  allied  to  premature 
beats  in  the  manner  of  its  production. 


(     75     ) 


Chapter  VI  I. 


AURICULAR    FLUTTER. 

The  term  "  auricular  flutter  "  is  used  in  this  chapter  to 
designate  extreme  acceleration  of  the  auricle.  I  employ 
it  when,  during  periods  of  acceleration,  the  auricular  rate  is 
maintained  above  200  per  minute.  The  disorder  is  riot  easy 
to  diagnose  by  methods  other  than  the  electrocardiographic. 
The  distinction  between  "  flutter  "  and  the  condition  described 
in  the  last  chapter  under  the  term  "  simple  paroxysmal 
tachycardia  "  may  ultimately  prove  too  arbitrary  ;  never- 
theless it  has  present  advantages,  for  although  the  two 
conditions  so  separated  have  a  number  of  features  in  common, 
yet  in  certain  ways  they  do  not  behave  alike.  From  the 
purely  clinical  standpoint  their  distinction  at  the  present 
time  is  of  decided  importance. 

The  usual  rate  of  auricular  contraction  in  flutter  is 
approximately  300  per  minute  ;  it  may  reach  330  per  minute. 
The  flutter  comes  abruptly  and  goes  abruptly,  as  does  a 
simple  paroxysm  of  tachycardia  ;  the  two  conditions  have 
this  common  characteristic  and  almost  certainly  possess  a 
common  pathological  basis.  Rarely,  flutter  also  occurs  in 
short  paroxysms,  but  in  general  it  persists  for  months  or 
years.  In  this  respect  "  flutter  "  has  an  affinity  with  another 
disorder,  namely  "  auricular  fibrillation,"  which  is  described 
in  the  next  chapter. 


76 


Chapter  VII. 


The  auricular  rate  is  so  rapid  that  the  ventricle  is  rarely 

able  to  follow  it  ;     so  it  happens  that  most  patients  who 

exhibit   flutter  also   demonstrate   heart-block,   the   grade   of 

which  is   generally  such   that   only  the   alternate   auricular 

impulses  stimulate  the  ventricle.     Most  patients  who  are  the 

subjects  of  flutter  have  an  enhanced  ventricular  rate,  but  the 

ventricular  rate  is  but  one  half  the  auricular.     On  the  other 

hand,  the  ventricular  rate  may  be  slow  ;    any  grade  of  block 

may  be  present. 

The  electrocardiograms. 

The  electrocardiograms  are  not  difficult  to  recognise  if 

carefully  examined.     It  is  often  of  advantage  to  have  the 


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Fig.  64.  Curves  from  the  three  leads  in  a  case  of  auricular  flutter.  The 
auricular  rate  is  324,  the  ventricular  rate  is  162  per  minute.  In  leads  II 
and  III  the  auricular  complexes  are  contiguous. 

curves  from  the  three  leads  side  by  side,  so  that  similar  events 
may  be  compared  in  distinct  leads.  Fig.  64,  which  comprises 
all  three  leads,  may  be  used  to  illustrate  the  chief  points  in 
the  analysis.  In  lead  //of  this  figure  the  most  conspicuous 
peak  is  R  ;  it  is  followed  by  a  small  depression  8.  These  are 
the  only  certain  indications  of  ventricular  systole.  The 
remainder  of  the  curve  may  be  described  as  consisting  of 


Auricular  Flutter.  77 

two  V-shaped  depressions,  one  of  which  might  seem  to 
correspond  to  an  inverted  T,  the  other  to  an  inverted  P. 
The  two  depressions  have  an  almost  exactly  similar  shape. 
Now  this  is  not  inconsistent  with  their  representing  an 
inverted  P  and  T,  for  similarity  of  the  two  deflections  is  not 
uncommon.  But  it  would  be  a  strange  coincidence  if,  with 
this  similarity,  P  and  T  should  be  placed  at  exactly  equal 
distances  from  each  other  throughout  the  whole  curve. 
Moreover,  even  though  P  and  T  may  resemble  each  other  in  a 
given  lead,  they  never  do  in  all  three  leads  ;  yet  in  each  of 
the  curves  of  our  illustration  a  uniform  series  of  waves  is 
present.  In  lead  III  they  are  of  much  the  same  form  as  in 
lead  //  ;  while  in  lead  /  they  appear  as  small  peaks.  In  all 
leads  they  lie  at  equal  distances  from  adjacent  summits  of 
the  same  form  ;  in  all  leads  the  deflections  lie  in  orderly 
sequence.  These  facts  demonstrate  that  the  two  waves 
have  a  similar  origin  ;  and,  although  alternate  waves  lie  in 
ventricular  diastole,  all  are  the  result  of  auricular  systoles. 
Fig.  64  therefore  shows  2  :  1  heart-block,  the  rate  of  the 
auricle  being  324  and  that  of  the  ventricle  162.  In  leads 
//  and  III  the  real  T  is  scarcely  distinguishable,  but  in 
lead  /  it  is  clear,  having  a  broad  form  and  falling  between 
two  P  summits. 

The  electric  representatives  of  auricular  contractions, 
when  this  chamber  is  in  a  state  of  flutter,  are  usually  con- 
tiguous. In  Fig.  64  this  is  clearest  in  lead  //.  P  com- 
mences in  an  upstroke  but  is  continued  in  a  dome  which 
ends  at  the  foot  of  the  succeeding  upstroke.  As  one  upstroke 
precedes  R,  so  the  dome  into  which  it  continues  runs  through 
R  and  S.  The  next  dome  commences  during  the  ventricular 
systole  and  runs  on  into  ventricular  diastole.  Each  auricular 
contraction  partially  coincides  with  a  ventricular  contraction 
and  it  is  to  this  that  this  and  many  other  flutter  curves 
owed  their  original  obscurity.     Other  examples  of  curves  are 


78 


Chapter   VII. 


shown  in  Fig.  65,  66  and  67.  Fig.  65  shows  the  common 
type  of  auricular  curve.  The  auricular  contractions  are  again 
twice  as  numerous  as  the  ventricular.  Each  auricular 
complex  consists  of  an  upstroke  at  its  commencement,  but 
this  upstroke  is  only  clearly  distinguished  where  it  precedes  R. 
It  continues  to  a  blunt  summit  and  then  the  curve  slopes 
away  and  becomes  incorporated  in  the  ventricular  complex. 
The  next  upstroke  coincides  with  the  returning  line  of  S  ; 


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Fig.    65,    66  and   67.      Examples  of  auricular  flutter  curves.     In  each  2  :  1 

heart-block    is    present.     The    auricular    rates    are    approximately  330, 

280   and   228,   respectively;     the  ventricular  rates,'  165,    140   and  114, 
respectively. 


it  comes  to  a  point  and  slopes  away  again,  but  the  gradual 
downstroke  is  interrupted  by  a  small  T  summit.  Thus  the 
auricular  tracing  as  a  whole  is  constituted  by  a  zig-zag  line 
of  which  the  upstrokes  are  steep  and  the  downstrokes  are 
more  gradual. 

Fig.  66  exhibits  a  similar  action.  The  ventricular 
complexes  consist  of  R  and  S  deflections.  The  auricular 
portion  of  the  curve  is  traced  as  a  uniform  wavy  line  ;    one 


Auricular  Flutter.  79 

-convexity  falls  midway  between  R  summits,  the  other  falls 
with  R.  The  general  and  uniform  undulation  is  visible 
though  disguised  ;  each  convexity  represents  an  auricular 
contraction  ;  2:1  heart-block  is  present.  The  rates  of 
auricle  and  ventricle  are  280  and  140,  respectively. 

The  analysis  of  Fig.  67  is  easier,  for  here  the  P's  are 
isolated.  Their  isolation  is  due  to  the  lower  rates  (auricle 
228,  ventricle  114).  The  analyses  while  2:  1  heart-block  is 
present  are  difficult  to  those  unfamiliar  with  the  curves  ; 
sometimes  the  analysis  is  impossible  at  this  stage.  The  true 
nature  of  the  condition  is  at  once  revealed  when  a  higher 
grade  of  heart-block  becomes  established.  The  first  curve 
of  Fig.  72  is  not  very  dissimilar  to  that  of  Fig.  66.  The 
auricular  line  is  a  wavy  one  and  there  are  two  convexities  to 
each  ventricular  systole  ;  one  falls  midway  between  adjacent 
R  summits,  the  other  coincides  with  R  ;  2:1  heart-block  is 
present,  the  rates  being  300  and  150.  The  same  patient 
demonstrated  a  higher  grade  of  block  upon  another  day  ;  the 
auricular  convexities  then  became  clear,  being  less  confused 
with  the  ventricular  summits  ;  the  curve  is  shown  in  the 
second  strip  of  Fig.  72  ;  4:1  block  is  present,  the  rates  being 
300  and  75.  (Similar  electrocardiograms  are  shown  in  the 
first  two  curves  of  Fig.  73,  the  top  curve  of  which  should  be 
compared  with  Fig.  65.)  The  same  4  :  1  ratio  is  shown  in 
Fig.  68,  a  curve  which  has  been  taken  at  a  faster  speed  and 
with  a  more  sensitive  string.  This  curve  has  been  marked 
:so  as  to  reconstruct  that  portion  of  the  auricular  line  which 
is  obliterated  by  R  and  8  ;  the  regular  relation  of  four 
auricular  convexities  to  a  ventricular  systole  is  made  more 
apparent  in  this  way. 

The  continuous  activity  of  the  auricle  may  be  demon- 
strated in  another  way.  If  the  vagi  are  pressed  upon  in  the 
neck,  the  ventricular  beating  is  often  checked  ;  but  the 
-auricle  continues  to  contract  at  its  former  rate   (Fig.   69). 


80  Chapter  VII. 

The  continuously  wavy  line,  each  convexity  of  which  stands 
for  an  auricular  beat,  is  thus  strikingly  displayed. 

That  the  active  centre  in  the  auricle  is  ectopic  is  rendered 
probable,  though  it  still  remains  uncertain,  by  comparing" 
flutter  curves  with  those  of  the  normal  rhythm  in  the  same 
cases.  Examples  are  shown  in  the  first,  second  and  fourth 
strips  of  both  Fig.  72  and  Fig.  73.  In  the  first  strips  of  Fig.  72" 
the  auricular  beat  displays  a  simple  convexity.  In  the  last 
strip,  in  which  the  normal  rhythm  is  present,  it  gives  a  short 
summit  followed  by  a  depression.     In  the  first  two  strips  of 


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Fig,  68.  From  a  case  of  flutter,  showing  4  :  1  heart -block.  Those  portions- 
of  the  auricular  complexes  which  have  been  obscured  by  the  initial 
phases  of  the  ventricular  complexes  have  been  indicated  by  reconstructing 
the  auricular  oscillations.  The  standard  for  this  curve  is  1|  centimetres- 
to  the  millivolt. 


Fig.  73  the  auricular  beats  are  of  the  same  shape  as  those  of 
Fig.  65  ;  there  is  an  abrupt  upstroke  and  more  gradual 
downstroke  ;  the  normal  type  of  auricular  complex  for  this- 
case  (lead  ///)  is  inverted*  and  split.  The  ectopic  nature- 
of  the  flutter  impulses  is  also  suggested  from  another  source. 
Ectopic  centres  are  far  less  under  control  than  is  the  normaL 
pacemaker.  In  the  case  of  simple  paroxysms  of  tachycardia,, 
in  which  the  fast  rhythms  are  known  to  be  ectopic,  nerve- 
influences,  such  as  are  induced  by  exercise,  emotion,  posture^ 


*  Inversion  of  P  in  lead    ///  does  not  necessarily  signify  an  ectopic; 
source  of  impulse  formation. 


Auricular  Flutter. 


81 


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82  Chapter   VII. 

or  pressure  upon  the  carotid  sheath  are  practically  without 
influence  upon  the  rate  at  which  the  impulses  are  generated. 
The  same  statements  apply  a  fortiori  to  flutter.  Fig.  69  and 
70  were  taken  from  the  same  patient  and  show  the  effects  of 
pressure  on  the  carotid  sheath,  during  the  flutter  stage  and 
during  the  stage  of  normal  heart  action.  In  both  cases  the 
vagus  has  been  stimulated,  as  is  shown  in  the  one  instance  by 
ventricular  standstill  and  in  the  other  by  slowing  of  the  whole 
heart  with  a  slight  prolongation  of  the  P-B  interval.  Both 
curves  afford  evidence  of  heart-block  as  a  result  of  pressure, 
but  the  essential  difference  lies  in  the  action  upon  the  auricle. 
The  flutter  centre  is  uninfluenced  (Fig.  69)  ;  the  old  centre 
reacts  ;  the  rate  at  which  it  builds  up  impulses  being 
conspicuously  decreased  (Fig.  70). 

Auricular  flutter  occurs  for  the  most  part  in  elderly 
subjects  and  in  those  in  whom  there  are  evidences  of  cardiac 
enlargement,  myocardial  degeneration,  and  symptoms  of  an 
exhaustion  of  reserve.  When  it  develops,  it  throws  a  burden 
upon  the  heart  proportioned  to  the  increase  of  ventricular 
rate.  When  the  heart  muscle  is  degenerate  and  the  rate 
rapid,  dilatation,  engorgement  of  the  veins,  enlargement  of 
the  liver  and  dropsy  appear.  On  the  other  hand,  when  it 
develops  in  a  heart  whose  muscle  has  considerable  reserve, 
profound  circulatory  disturbances  and  embarrassment  are 
not  manifested  ;  but  palpitation  is  common  and  a  retrench- 
ment of  reserve  power  in  the  response  to  effort  is  noticeable. 
In  this  manner  it  disables  even  those  in  whom  the  heart 
muscle  is  strong.  Fainting  attacks  are  not  uncommon  in  the 
condition,  and  are  due  to  the  ventricle  suddenly  responding 
to  the  full  auricular  rate. 

Flutter  may  pass  spontaneously  into  fibrillation,  but 
more  commonly  the  change  is  induced  by  digitalis  adminis- 
tration. Digitalis  and  its  allies  are  often  very  serviceable 
if  given  in  full  doses  and  the  reaction  is  highly  interesting. 


Auricular  Flutter. 


83 


In  my  experience,  the  ventricular  rate  can  always  be  reduced, 
so  that  2  :  1. block  gives  place  to  heart-block  of  higher  grade. 
Supposing  2  :  1  heart-block  is  present  originally,  then 
irregularity  develops,  and  this  is  due  to  responses  at  irregular 


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72.  Four  curves  from  a  case  of  long  standing  auricular  flutter,  showing 
the  effects  of  treatment.  The  first  curve  shows  an  auricular  rate  of  300 
and  a  ventricular  rate  of  150.  In  the  second  curve  the  auricular  rate  is 
maintained,  but  the  ventricular  rate  has  been  halved  (4  :  1  block  is  present) 
as  a  result  of  digitalis  administration.  In  the  third  curve  auricular 
fibrillation  is  seen  and  it  is  accompanied  by  a  slow  and  irregular  action 
of  the  ventricle.  In  the  last  curve  the  normal  rhythm,  interrupted  by 
occasional  premature  contractions  of  auricular  origin,  has  been  restored. 

intervals  (Fig.  71).  Later,  and  if  the  drug  is  continued,  the 
ventricle  may  become  regular  again,  as  a  result  of  the 
development  of  4  :  1  block  (Fig.  72  and  73).  Under  these 
circumstances  the  ventricle  may  be  beating  at  75  while  the 

G    2 


84 


Chapter   VII. 


auricles  continue  to  beat  at  300  per  minute,  and  there  may 
be  no  evidence,  except  the  electrocardiographic,  of  the  rapid 
auricular  beats.  Finally,  and  in  a  large  percentage  of  cases, 
I  find  that  fibrillation  of  the  auricles  appears  under  the 
action  of  the  drug  (Fig.  72  and  73)  ;  and  further  that,  if  the 
digitalis  is  withdrawn  at  this  stage,  the  normal  action  of  the 


-  •  •  • rr. 


Fig.  73.  A  similar  series  of  curves  to  that  shown  in  Fig.  72.  They  show  the* 
effects  of  digitalis  administration  upon  long  standing  auricular  flutter.  In 
the  first  curve  the  auricular  rate  is  320  and  the  ventricular  rate  is  160.  In 
the  second  the  rates  are  324  and  81  (4  :  1  heart-block).  In  the  third,  the 
auricles  are  fibrillating  and  the  ventricle  is  responding  irregularly  at  an 
approximate  rate  of  79  per  minute.  In  the  last  curve  a  regular  and 
normal  rhythm  is  established.  The  inversion  of  P  in  lead  III  is  not 
significant  of  an  ectopic  origin  of  the  heart  beat  in  this  instance. 

heart  is  restored  (Fig.  72  and  73)  and  may  persist  for  years. 
The  treatment  of  auricular  nutter  by  digitalis  is  often 
most  successful  and  brings  with  it  great  improvement  of 
the  patient's  general  condition.  As  the  rapid  ventricular 
rate  subsides,  cyanosis,  engorgement,  dropsy  and  other 
accompanying  symptoms  vanish  quickly. 


(     85     ) 


Chapter   viii. 


AURICULAR    FIBRILLATION. 

Fibrillation  of  the  auricles,  a  state  in  which  co-ordinate 
contraction  has  ceased  in  these  heart  chambers  and  in  which 
the  surface  of  the  muscle  exhibits  constant  minute  twitching 
movements,  is  the  supreme  disorder  of  the  heart  beat  which 
is  compatible  with  life.  The  muscle  of  the  auricles,  though 
extremely  active,  has  relinquished  its  function  of  driving 
blood  into  the  ventricles  ;  the  normal  impulses  which  are 
transmitted  to  the  ventricle  are  submerged  and  replaced 
by  rapid  impulses  which  are  derived  in  a  haphazard  fashion 
from  the  quivering  muscle  of  the  auricle. 

Our  ability  to  recognise  this  disorder  is  a  great  asset 
because  it  is  so  frequent,  because  its  effects  are  so  profound, 
and  because  its  reactions  to  treatment  are  almost  peculiarly 
its  own.  The  electric  curves  of  auricular  fibrillation  are 
characteristic  and  afford  the  only  certain  means  of  identifying 
it.  It  is  recognised  by  two  groups  of  signs  ;  the  first  signs 
result  from  the  changed  functional  state  of  the  auricles, 
the  second  signs  depend  upon  the  character  of  the  ventricular 
responses.     We  will  consider  the  last  first. 

When  the  ventricle  responds  solely  to  a  fibrillating 
auricle,  its  beats  are  necessarily  of  supraventricular  origin  ; 
they  consequently  present  the  normal  outlines  in  electric 
curves,  R  and  T,  or  Q,  R,  S  and  T  deflections  are  found. 
These  ventricular  complexes  have  all  the  same  general  outline, 


86  Chapter   VIII. 

though  the  heights  of  the  R  summits  vary  in  many  cases 
from  cycle  to  cycle.  If  the  ventricular  action  is  slow,  then 
the  R  summits  are  almost  constant  in  height,  but  when  it  is 
rapid  (Fig.  74  and  75)  the  excursions  vary,  and  there  is  then 
no  relation  between  their  heights  and  the  diastoles  which 
precede  them  ;  the  individual  complexes  are  placed  at  very 
irregular  intervals.  The  other  group  of  signs  is  auricular. 
The  R  summits  have  no  P  summits  before  them,  for,  as  there 
is  no  co-ordinate  contraction  of  the  auricle,  so  there  is  no 


Fig.  74.  A  curve  of  auricular  fibrillation  showing  rapid  and  irregular 
ventricular  responses.  The  height  of  the  peak  R  is  variable  and  is  not 
related  to  the  length  of  the  diastole  which  precedes  it.  The  oscillations 
are  obscured  by  the  rapid  ventricular  action  ;  that  they  are  present  is 
evident  from  the  changing  shape  of  those  parts  of  the  curve  which  unite 
adjacent  R  summits.     There  are  no  P  summits. 

Fig.  75.  A  curve  of  auricular  fibrillation,  showing  rapid  and  irregular 
ventricular  response,  great  variation  in  the  height  of  R,  and  inversion  of 
T.  Fibrillation  oscillations  are  only  just  visible  ;  the  very  rapid  and 
minute  vibrations  are  from  the  body  musculature.  There  are  no  P 
summits. 

presystolic  auricular  representative  in  the  electric  curve  ; 
but  the  quivering  flesh  of  the  auricle  yields  pronounced 
electric  waves,  oscillations  which  characterise  the  majority 
of  the  curves.  The  type  of  chief  oscillation  deserves  study  ; 
the  approximate  frequence  is   500  per  minute  ;     so,  if  the 


Auricular  Fibrillation.  87 

ventricle  beats  at  83,  there  will  be  about  six  oscillations  to 
each  cycle,  or  if  it  beats  at  125,  there  will  be  about  four 
oscillations  to  each  cycle.  Only  those  oscillations  which 
occupy  diastole  are  prominent  ;  consequently,  if  the  ventricle 
beats  slowly,  the  oscillations  are  conspicuous  ;  but  if  it 
beats  fast,  they  may  be  difficult  to  distinguish. 

The  oscillations  of  the  first  curve  in  Fig.  80  are  very  large, 
and  it  should  be  remarked  that  there  is  an  attempt  towards 
regular  disposition,  but  the  individual  swings  of  the  fibre 
are  never  quite  uniform  as  in  flutter.     When  T  is  prominenti- 
as in  this  curve,  it  is  deformed  by  oscillations  which  fall  with 
it.   The  oscillations  are  continuous,  but  in  one  place  (between 
the  third  and  fourth  R  summits)  the  amplitude  is  diminished. 
This  variation  is  always  present,  and  if  the  mean  amplitude 
is  small,  then  the  oscillations  may  vanish  from  place  to  place  in 
the  curves.    In  Fig.  81  (top  curve)  they  are  prominent  at  the 
beginning,  but  towards  the  end  they  are  barely  perceptible. 
When  the  ventricle  beats  fast,  as  in  Fig.  74  and  75,  diastole 
is  comparatively  short  and  they  are  not  clearly  seen.     Their 
presence  is  ascertained  in  such  curves  by  scrutinising  the 
lines  which  join  the  R  summits  ;    these  lines  are  differently 
configured    from    cycle    to    cycle.     The    oscillations    are    in 
reality  quite  continuous,  but,  as  in  flutter  curves  (Fig.  65  and 
66),    fast    ventricular    action    obscures    them.     They    are 
especially  prominent  in  cases  of  mitral  stenosis  (Fig.  80  and 
94).     In  other  conditions  they  are  often  small  ;   Fig.  76  is  an 
example   of   such   a   curve  ;     this   electrocardiogram   should 
immediately  suggest  fibrillation,  for  the  ventricular  complexes 
are  all  of  the   supraventricular  type,  and  quite  irregularly 
spaced  ;     furthermore,    there    are    no    P    summits.     There 
are  deflections  in  Fig.    74  which  at  first  suggest  auricular 
contractions,  but  they  are  inconstant  in  form  and  position 
and   should   not    mislead,    being    in   reality   individual   and 
prominent  oscillations  which  happen  to  fall  in  presystole. 


88 


Chapter   VIII. 


Fig.  77  shows  another  and  distinct  form  of  oscillation  ;  it  is  of 
very  high  frequence  and  due  to  tremor  of  the  somatic  muscles  ; 


mam  mm  i  bb  bbb i  bh  i  i  a  1 1 1  i  a  i  n  a  i  f  i  n  1 1 1 1  n  1 i  liMiUMMtokiWMu-vHuim 


Fig.  76.  From  a  case  of  fibrillation  under  treatment  with  digitalis.  It 
shows  irregularity  of  the  ventricle  and  inversion  of  T.  The  oscillations 
are  small  ;    P  does  not  appear. 


Fig.  77.  From  a  case  of  fibrillation  under  treatment  with  digitalis.  The 
ventricular  action  is  irregular.  The  diastolic  portion  of  the  curve  shows 
two  series  of  oscillations,  the  one  (/./.)  due  to  the  fibrillation  of  the 
auricle,  the  other  resulting  from  tremor  ;  these  last  oscillations  have  a 
very  high  frequence. 


Fig.  78.  From  a  case  of  exojmthalmic  goitre,  showing  a  regular  heart  action. 
Each  ventricular  complex  is  preceded  by  a  summit  P,  but  the  whole 
curve  is  disturbed  by  oscillations  resulting  from  tremor  of  the  somatic 
musculature. 


Fig.  79.  From  a  case  of  auricular  fibrillation,  under  treatment  with  digitalis. 
The  fibrillation  is  evidenced  by  the  oscillations  /../.  and  by  the  dis- 
appearance of  P  summits.  The  ventricular  beats  are  placed  regularly 
because  complete  heart-block  was  present.  The  rate  is  exceptional  for  a 
ventricular  rhythm,  being  approximately  90  per  minute. 


Auricular  Fibrillation.  80 

It  is  not  to  be  ascribed  to  fibrillation,  although  the  curve 
was  actually  from  a  case  displaying  this  disorder.  These 
minute  vibrations  are  common  in  fibrillation  cases,  for  the 
patients  are  often  feeble  or  actually  tremulous,  but  they  may 
be  present  when  no  tremor  is  detected  and  may  then  confuse 
interpretations.  It  is  wise  to  neglect  them  and  to  look  to  the 
general  sweep  of  the  curve.  In  Fig.  77  they  are  present 
throughout  and  distort  the  curve  ;  it  is  from  a  fibrillation  case, 
-as  may  be  seen  immediately  from  the  shape  of  the  ventricular 
complexes,  their  arrangement  and  the  absence  of  P  summits  ; 
if  the  curve  is  regarded  with  the  eyelids  almost  closed,  the 
fine  tremor  is  no  longer  distinguished  and  the  slower  and 
inconspicuous  oscillations  of  the  fibrillating  auricles  then 
become  clearer  ;  these  are  most  prominent  after  the  second 
ventricular  beat  and  have  the  characteristic  form.  Fig.  78, 
&  different  type  of  curve,  illustrates  the  same  distinction  ; 
it  is  from  a  case  of  exophthalmic  goitre  in  which  there  was 
much  tremor.  The  tremor  oscillations  are  large  and  coarse, 
serrating  the  whole  curve  and  obscuring  P  ;  nevertheless  P 
or  some  trace  of  it  may  be  discovered  in  each  cycle,  despite 
the  distortion  ;  it  should  be  noted  also  that  the  ventricular 
oeats  are  evenly  distributed.  The  action  of  the  heart  from 
which  this  curve  was  taken  was  normal.  Sometimes,  when 
the  somatic  muscle  tremor  is  coarse  and  the  patient  holds 
the  limbs  rigidly  or  unsteadily,  the  curves  present  difficulties 
and  there  may  be  doubt  as  to  whether  a  given  series  of 
oscillations  is  of  somatic  or  cardiac  origin  ;  under  these 
conditions  special  leads  may  profitably  be  adopted.  Small 
metallic  discs  are  fastened  directly  to  the  chest  wall  with  a 
stiff  paste  of  flour  and  salt.  Convenient  points  of  contact 
are  depicted  in  the  accompanying  diagram  which  illustrates 
the  method  (Fig.  80).  When  fibrillation  is  present  and  the 
electrodes  lie  in  the  vicinity  of  the  right  auricle  (leads  1  and  2 
of  the  diagram)  the  oscillations  are  maximal,  and  there  is  but 


90 


Chapter   VIII. 


iiiiimitfimHtiiniHiiiiiniiiim'.  -.  'fm^miu-mtmnut  .■ .  ..tummaa 


x  \gSg&P  TEjm^ijjgmmt 


....„.......,»M., ,.,..,  ...,.,...,.,,»...»„..,«.,«..^^.^.». ,. MM.MMM^M.MM»UJ^miam«i.M.M» 

-big.  80.  A  diagram  of  the  chest  wall  showing  the  special  leads  (1  to  5) 
used  in  identifying  the  oscillations  of  auricular  fibrillation  ;  also  six 
electrocardiograms.  The  first  electrocardiogram  is  from  lead  II ;  it 
consists  of  irregularly  placed  ventricular  complexes  {R,  T)  and  of  large- 
and  continuous  oscillations  (/./).  The  remaining  five  curves  are  from 
the  chest  wall.  1  and  2  were  taken  from  the  area  overlying  the  right 
auricle  ;  in  these  leads  the  oscillations  are  maximal  and  the  ventricular- 
complexes  are  minimal.  3  was  taken  from  an  oblique  lead  covering  the 
whole  heart,  and  it  shows  both  oscillations  and  ventricular  complexes. 
4  and  5  were  taken  from  leads  along  the  margins  of  the  ventricles  ;  they 
show  but  little  sign  of  the  oscillations.     From  a  case  of  mitral  stenosis. 


Auricular  Fibrillation.  91 

a  trace  of  the  ventricular  beats.  When  they  lie  in  the  long 
axis  of  the  heart  (lead  3)  both  the  oscillations  and  the 
ventricular  complexes  are  conspicuous.  Finally,  when  they 
lie  along  the  left  or  right  ventricular  border  (leads  4  and  5) 
the  ventricular  complexes  are  clear  cut  while  the  oscillations 
are  small  or  absent.  The  corresponding  electrocardiograms 
are  shown  below  the  diagram,  the  first  curve  of  which  is  from 
the  customary  lead  //  (right  arm  to  left  leg).  The  special 
contacts  analyse  this  axial  lead,  breaking  it  into  its  auricular 
and  ventricular  constituents.  The  oscillations  of  fibrillation 
are  readily  identified  in  this  manner  and  their  origin  in  the 
auricle  is  clearly  indicated.  In  tremulous  subjects,  oscillations 
are  not  seen  in  leads  from  the  chest  unless  the  muscles  of  the 
chest  are  visibly  twitching. 

The  chief  features  of  the  electrocardiograms  in  fibrillation 
of  the  auricle  are  strikingly  displayed  when  the  curves  of  this 
condition  and  those  showing  the  normal  rhythm  can  be 
compared  in  one  and  the  same  case.  Fibrillation,  though 
usually  a  chronic  and  persistent  disorder,  occasionally  occurs 
in  short  paroxysms  or,  as  we  have  seen,  terminates  a  period 
of  auricular  flutter.  In  such  patients  the  comparison  is 
possible.  The  curves  of  Fig.  81  were  taken  from  the  same 
patient  within  a  few  days  of  each  other.  The  ventricular 
complexes  are  of  the  same  type  in  both  ;  in  one  they  are 
distributed  regularly  and  are  preceded  by  the  usual  P  summits 
(second  curve)  ;  in  the  other  the  spacing  is  irregular,  no  P 
summits  are  discovered,  and  the  whole  base  line  exhibits  the 
oscillations  of  fibrillation   (first   curve). 

Two  groups  of  signs  have  been  insisted  upon,  namely,  the 
auricular  and  ventricular,  respectively.  In  the  great  majority 
of  curves,  the  signs  of  both  groups  are  found.  We  may  now 
discuss  the  exceptional  curves.  It  has  been  said  that  the 
oscillations  may  almost  fail  ;  absolute  failure,  if  it  occurs, 
is  so  rare  that  it  needs  little  consideration.     More  important, 


92 


Chapter   VIII. 


Auricular  Fibrillation.  93 

from  the  standpoint  of  diagnosis,  is  the  association  of 
auricular  fibrillation  with  regular  action  of  the  ventricle. 
This  combination  is  also  very  infrequent,  but  occurs  when  the 
auricular  impulses  no  longer  control  the  ventricle  ;  in  other 
words,  when  the  last-named  chamber  beats  independently. 
Being  exceptional,  it  serves  to  emphasise  the  rule,  that  while 
auricular  fibrillation  is  present,  the  ventricular  movements 
are  disorderly.  Fig.  79  illustrates  the  condition  ;  it  shows  the 
usual  type  of  oscillation,  no  auricular  summits  P  are  seen,  but 
the  ventricular  beats  have  natural  outlines  and  are  in  regular 
sequence.  It  is  desirable  to  confirm  the  origin  of  the  oscilla- 
tions in  these  patients  by  means  of  the  chest  wall  leads. 

Fibrillation  is  the  acme  of  auricular  disturbance,  con- 
sequently it  is  never  complicated  by  other  perversions  of 
auricular  rhythm.  But  the  heart  which  exhibits  it  may 
display  any  other  type  of  disorder  at  the  same  time. 
Thus  there  may  be  heart-block.  The  responses  of  the 
ventricle  to  a  fibrillating  auricle  are  naturally  rapid  and 
approach  200  per  minute.  A  slower  ventricular  action 
indicates  heart-block,  and  the  degree  of  heart-block  is 
gauged  by  the  degree  of  slowing.  It  is  by  producing  high 
grades  of  partial  heart-block  and  by  assuaging  the  original 
rapidity  of  the  ventricular  beats  that  digitalis  and  its  allies 
produce  their  most  notable  clinical  effect.  Fig.  76  and  77 
were  taken  from  patients  fully  under  the  influence  of  these 
drugs  ;  the  ventricular  rates  were  47  and  52  when  the  curves 
were  taken  ;  before  treatment  they  had  been  rapid.  Digitalis 
heart-block  may  be  complete  (Fig.  79  is  an  example)  and 
when  complete  from  this  cause,  the  rate  of  the  regular 
ventricle  is  relatively  high.  Heart-block  resulting  from 
bundle  lesions  produces  slow  ventricular  action  when  the 
auricles  fibrillate,  and  when  complete,  the  ventricular  rates 
are  of  the  same  order  as  those  of  uncomplicated  heart-block. 
Thus  fibrillation  may  be  accompanied  by  ventricular  rates 


94 


Chapter  VIII. 


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Auricular  Fibrillation.  95 

which  range  from  30  to  200,  according  to  the  conducting  power 
of  the  auriculo- ventricular  bundle. 

The  ventricular  complexes  in  fibrillation  are,  as  has  been 
said,  of  the  supraventricular  type,  but  T  may  show  inversion 
(Fig.  76)  and  the  aberrant  forms  of  beat,  described  on  page  27, 
may  occur,  when  one  or  other  bundle  branch  is  damaged. 
The  comparative  amplitudes  of  R  and  S  in  the  three  leads  have 
the  same  significance  as  they  have  when  the  sequence  is 
normal  (see  page  30  and  Fig.  94). 

Extrasystoles  are  seen  from  time  to  time  ;  they  spring 
irom  ventricular  foci.*  An  example  of  this  kind  is  given  in 
Fig.  82  ;  this  curve  was  taken  from  lead  ///  and  the 
diminutive  E  and  deep  S  are  indications  of  left  ventricular 
hypertrophy  ;  a  single  anomalous  contraction,  a  premature 
T)eat,  is  seen  towards  the  end  of  the  figure,  and  its  form  in  the 
electric  curve  is  that  of  a  beat  arising  in  the  left  ventricle. 
These  premature  beats  are  recorded  most  often  in  patients 
^who  are  taking  digitalis  or  the  allied  drugs ;  appearing  in 
these  circumstances,  they  suggest  relaxation  of  the  treatment. 
When  more  frequent,  they  constitute  urgent  messages 
that  the  drug  be  discontinued  ;  the  condition  is  exemplified 
"by  Fig.  83  ;  it  is  known  as  "  digitalis  coupling."  Each 
ventricular  complex  of  the  supraventricular  type  (B,  T) 
is  followed  at  a  close  and  constant  interval  by  a  complex 
•of  anomalous  form.  In  this  instance,  the  form  is  that  of 
beats  coming  from  the  right  ventricle.  The  ventricular  rate 
is  slow  ;  there  are  no  P  summits,  but  there  are  small  oscilla- 
tions during  the  diastolic  periods.  The  auricle  is  fibrillating. 
A  continuation  of  digitalis,  when  this  coupling  has  declared 
itself,  is  culpable  ;  it  is  followed  only  too  frequently  by  sudden 
and  avoidable  disaster. 


*  Almost  exclusively  so  ;    naturally  they  cannot  originate  in  the  auricle, 
Ibut  some  appear  to  originate  in  the  junctional  tissues. 


(     96     ) 


Chapter  IX. 


SINUS    DISTURBANCES     AND     ALTERNATION. 
Respiratory  arrhythmia  and  allied  irregularities. 

There  are  a  number  of  closely  related  heart  irregularities y 
which  are  due  to  variations  in  the  rate  at  which  the  impulses 
are  generated  at  the  physiological  pacemaker.  A  notable 
example  is  an  irregularity  of  respiratory  origin  (Fig.  84) 
in  which  there  is  a  gradual  acceleration  during  the  inspiratory 
phase  and  a  fall  of  rate  during  the  expiratory  phase  of 
respiration.  In  young  subjects  it  is  a  normal  phenomenon  ; 
and  during  the  earlier  periods  of  life,  allied  irregularities,  in 
which  the  whole  heart  participates  but  in  which  there  is  no 
constant  relation  to  the  acts  of  breathing,  are  observed 
(Fig.  85).  These  irregularities,  often  grouped  under  the- 
term  "  sinus  arrhythmia,"  are  brought  about  by  alterations 
of  vagal  tone.  In  electrocardiograms  they  are  readily 
recognised.  Each  beat  of  the  heart  is  propagated  from  the 
natural  pacemaker  ;  the  electric  curve  is  consecpaently  formed 
of  physiological  complexes,  in  which  the  usual  auricular  and 
ventricular  summits  are  seen.  The  disturbance  is  confined 
to  irregular  disposition  of  the  beats ;  the  normal  seepience  of 
chamber  contraction  is  retained. 


/Sinus    Disturbances  and  Alternatioi 


97 


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98  Chapter  IX. 

Sino-auricular  heart-block. 

There  is  another  though  infrequent  form  of  irregularity, 
which  is  related  to  those  just  considered.  Provisionally  it  is 
termed  "  sino-auricular  heart-block/'  This  irregularity  is 
but  imperfectly  understood  and  its  significance,  though 
apparently  inconsiderable,  is  not  fully  known.  In  many 
patients  it  is  of  vagal  origin  ;  it  is  not  uncommonly  associated 
with  auriculo-ventricular  heart-block  and,  like  the  latter, 
may  appear  during  digitalis  administration.  It  generally 
manifests  itself  in  one  of  two  ways — by  producing  inter- 
mittences  of  the  whole  heart,  or  by  leading  to  steep  falls  of 
heart  rate.  When  a  single  heart  beat  is  lost  (as  in  Fig.  86), 
the  length  of  the  longest  cycles  is  usually  somewhat  shorter 
than  two  cycles  of  the  natural  rhythm.  When  the  heart  rate 
falls,  the  passage  from  one  rate  to  the  other  is  abrupt  ;  there 
is  no  transitional  period  (Fig.  87)  ;  although  the  slow  rate 
may  be  almost  exactly  half  the  former  rate  (Fig.  87),  yet  more 
commonly  actual  halving  of  rate  is  hardly  attained.  Per- 
manent slow  action  of  the  whole  heart  may  be  due  to  this 
disorder  (Fig.  35),  which  is  supposed  to  be  due  to  some  form 
of  imperfect  conduction  between  the  natural  pacemaker 
and  the  main  mass  of  the  auricular  tissue  ;  but  whether  this 
is  the  true  explanation  or  not  remains  to  be  decided. 

The  electrocardiographic  curve  of  each  heart  beat 
presents  auricular  and  ventricular  complexes  of  forms 
known  to  be  associated  with  heart  beats  of  normal  origin. 

Alternation  of  the  heart. 

When  alternation  of  the  heart  is  present,  and  is  displaying 
itself  in  the  arterial  pulse,  the  electrocardiograms  do  not 
always  show  it.  If  the  heart  is  beating  slowly  and  alternation 
of  the  pulse  is  conspicuous,  the  several  ventricular  summits 
and  depressions  may  be  of  uniform  amplitude  from  beat  to 


Sinus    Disturbances  and  Alternation. 


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Chapter  IX. 


beat  (Fig.  88)  ;  nevertheless  alternation  may  be  conspicuous 
in  the  electrocardiograms  ;  it  is  seen  to  advantage  in  Fig.  63. 
In  this  figure  it  is  increased  after  the  premature  contraction. 
When  alternation  accompanies  paroxysms  of  tachycardia, 
traces  of  alternation  in  the  amplitudes  of  R  and  T  are  usual. 
The  left-hand  portion  of  Fig.  62  serves  as  an  illustration  ;  the 


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Fig.  S8.  Simultaneous  electrocardiogram  and  arterial  curve.  The  last 
shows  conspicuous  alternation,  but  in  the  electrocardiogram  it  is  not 
perceptible  (see  Fig.  62  and  63). 


alternation  is  confined  to  R  and,  though  of  minor  degree, 
is  quite  distinct.  Curiously  enough,  the  alternation  in 
electrocardiogram  and  pulse  is  not  always  parallel  ;  while 
the  small  R  summit  may  correspond  to  the  small  pulse  beat, 
yet  quite  as  frequently  (as  in  Fig.  62)  the  large  R  corresponds 
to  the  small  pulse  beat.  On  occasion  alternation  of  amplitude 
may  be  present  in  the  electrocardiogram  when  the  pulse  fails 
to  show  it. 


(    ioi    ) 


Chapter  X. 

SPECIAL    CONDITIONS. 

Electrocardiograms  in  valve  lesions. 

As  a  preliminary  it  should  be  stated  emphatically  that 
electrocardiography  has  little  to  do  with  valve  lesions.  The 
method  is  essentially  one  which  investigates  the  muscle  ; 
only,  therefore,  in  so  far  as  valve  lesions  affect  the  muscle 
do  they  influence  the  form  of  electric  curves.  Now  the 
degree  to  which  valve  lesions  upset  the  distribution  of  the 
mass  of  heart  muscle  is  a  question  upon  which  we  have  no 
final  evidence  ;  there  is  always  the  primary  difficulty  that 
whatever  may  have  affected  the  valves  may  also  have 
affected  the  contractile  substance.  The  indiscriminate 
assignment  of  hypertrophy  of  this  or  that  chamber  to  leakage 
at  this  or  that  valve  as  a  causal  agent  cannot  be  too  strongly 
deprecated.  However  boldly  it  may  be  asserted  in  a  given 
case  that  left-  or  right-sided  hypertrophy  is  the  result  of 
purely  mechanical  defects,  the  conclusion  in  the  individual 
case  is  often  impossible  of  proof.  We  know  that  free  aortic 
leakage  may  consort  with  a  light  or  heavy  musculature  ; 
we  know  that,  produced  under  strictly  aseptic  conditions, 
reflux  at  this  valve  is  generally  followed  by  but  relatively 
little  muscle  change  ;  again,  some  of  the  largest  human 
hearts  are  found  where  no  sign  of  valve  defect  or  other 
mechanical  disadvantage,  to  which  cardiac  embarrassment 


102 


Chapter  X. 


3E^ 


r. ............. 


Fig.   89.  Fig.  90  and  91. 

Fig.  89.  From  a  case  of  mitral  stenosis.  The  summit  P  is  large,  broad  and 
notched  in  lead  II.  The  initial  ventricular  peaks  of  lead  I  are  small. 
R  is  tallest  in  lead  ///. 

Fig.   90.     From  a  case  of  mitral  stenosis,  showing  a  tall  summit  P. 

Fig.  91.  From  a  case  of  mitral  stenosis,  showing  a  broad  and  notched 
summit  P. 


Fig.  92.  From  a  case  of  mitral  stenosis.  The  summit  P  is  large,  broad  and 
notched  in  lead  II.  R  is  of  least  amplitude  in  lead  I  and  of  greatest 
amplitude  in  lead  III  ;  S  is  of  greatest  amplitude  in  lead  /  (preponderance 
of  right  ventricle). 


Special   Conditions.  103 

might  be  attributed,  has  ever  been  discovered.  While 
alteration  in  the  muscle  as  a  sequel  to  pressure  changes 
cannot  be  denied,  yet  it  becomes  increasingly  clear  that  this 
hypothesis  has  in  the  past  outstripped  the  facts.  No 
question  of  cardiac  pathology  requires  more  critical  revision 
to-day.  Newer  and  more  accurate  methods  of  observation, 
untrammelled  by  tradition,  are  needed.  These  remarks 
are  a  necessary  prelude  to  those  which  follow  ;  for  if  we 
look  for  the  electrocardiograms  which  are  held  to  depict 
preponderance  of  the  right  ventricle  in  all  cases  of  mitral 
stenosis  or  those  of  preponderance  of  the  left  ventricle  in  all 
cases  of  aortic  disease,  our  expectations  will  not  be  fulfilled. 
The  sign  of  left  preponderance  may  appear  in  mitral  stenosis 
and  that  of  right  preponderance  in  aortic  disease  ;  and  the 
reason  for  that  which  may  be  regarded  as  a  discrepancy — 
but  which  in  reality  is  not  a  discrepancy — is  not  obscure  ; 
the  left  ventricle  may  preponderate  in  mitral  stenosis  as  the 
right  may  in  aortic  disease. 

Mitral  stenosis.  The  electrocardiograms  of  mitral 
stenosis  are  often  so  characteristic  that  the  valve  lesion  may 
be  diagnosed  from  these  curves  alone.  The  summit  P  has  an 
exaggerated  amplitude,  amounting  frequently  to  2,  3  or  even  4 
scale  divisions  (Fig.  89,  90,  and  91  and  92  ;  and  also  Fig. 
29,  52,  53  and  86)  ;  it  is  often  broad,  flattened  and  notched 
in  the  centre  (Fig.  89,  91  and  92).  The  ventricular  complexes 
generally  indicate  preponderance  of  the  right  muscle.  Often 
this  change  is  shown  conspicuously  (Fig.  92),  8  being 
exaggerated  in  lead  /  and  R  in  lead  ///.  Sometimes  the 
change  is  less  evident  ;  small  R  and  S  deflections  in  lead  / 
(Fig.  89)  are  not  uncommon.  When  the  auricles  are  fibril- 
lating  the  evidence  of  right  preponderance  remains  (Fig.  94), 
and  the  exaggerated  P  summits  are  replaced  by  exceptionally 
large  oscillations  (Fig.  74,  79,  80  and  94).  Oscillations  of 
great    amplitude    (Fig.    80)    are   never   seen   except   in   this 


104 


Chapter  X 


Fig.  93  From  a  paroxysm  of  tachycardia  in  a  case  of  mitral  stenosis. 
Preponderance  of  the  right  ventricle  is  indicated  :  the  P  summits  are 
small  because  the  paroxysm  arose  in  an  ectopic  auricular  focus. 


5e^ 


=^ 


m 


Fig.  94.  From  a  case  in  which  the  auricles  were  fibrillating.  Preponderance 
of  the  right  ventricle  is  indicated  in  the  ventricular  complexes.  The 
oscillations  are  prominent,  as  is  usual  in  mitral  stenosis. 

The  heart  of  this  patient  was  subsequently  obtained.  Mitral 
stenosis  was  found.  The  left  ventricle  weighed  105  and  the  right  ventricle 
128  grammes. 


Special   Conditions. 


105 


condition,  so  far  as  my  experience  goes.  When  new  auricular 
rhythms,  constituting  paroxysms  of  tachycardia,  occur  in 
mitral  stenosis,  the  ventricular  peaks  still  suggest  right 
preponderance,  but  the  P  summits  no  longer  occur  in  their 


tmmuuiuim  uuuutui luuuuuuin 


|'""|"" nniiiinininniini.uun 


Fig.  95.  From  a  patient  in  whom  aortic  regurgitation  was  present,  showing 
inversion  of  T  in  lead  II.  The  curve  is  exceptional  because  it  speaks 
for  preponderance  of  the  right  ventricle. 


Fig.   96.     From  a  case  of  aortic  regurgitation,  showing  the  flattening  of   T 
which  is  common  in  hearts  which  have  this  valve  lesion. 


usual  forms  (Fig.  93).  The  signs  I  have  described  often 
lead  to  a  correct  diagnosis  of  mitral  stenosis,  which  without 
the  signs  would  be  unrecognisable.  Especially  is  this  so  when, 
the  auricles  being  in  fibrillation,  the  presystolic  murmur 
fails  or  is  replaced  by  a  murmur  falling  in  early  diastole. 


106 


Chapter  X. 


The  records  are  not  infrequently  helpful  in  differentiating 
diastolic  murmurs  of  aortic,  pulmonary  and  mitral  origin 
(Steell's  and  Flint's  murmur). 

Aortic  disease.  The  curves  of  aortic  disease  are  varied 
in  form  ;  the  uncomplicated  valve  lesion  produces  little  or 
no  alteration.  In  a  dog  in  which  free  regurgitation  was 
produced,  the  electrocardiograms,  taken  before  and  some 
forty  days  after  operation,  showed  no  appreciable  change  ; 


Fig.  97.  From  a  patient  in  whom  aortic  regurgitation  was  present.  It. 
serves  to  emphasise  the  important  distinctions  between  two  series  of 
curves,  namely,  those  which  are  associated  with  left  preponderance  and 
those  which  indicate  a  deficiency  of  the  right  branch  of  the  auriculo- 
ventricular  bundle  (see  Chapter  III.). 


such  slight  change  as  was  exhibited  was  unstable  from  day 
to  day.  It  is  true  that  left  ventricular  preponderance  is  often 
indicated  in  the  curves  of  the  human  subject  (Fig.  19  and  20), 
but  it  is  not  shown  with  constancy  in  this  condition,  and  is- 
encountered  more  frequently  when  aortic  disease  is  absent. 
The  picture  of  right  preponderance  is  also  compatible  with, 
lesions  of  this  valve,  though  the  association  is  exceptional 
(Fig.  95).     A  large  excursion  of  R  in  lead  //  (Fig.  95  and  96),, 


Special   Conditions. 


107 


smallness  of  T  (Fig.  96)  or  inversion  of  the  same  summit  in 
lead  //  (Fig.  95)  are  quite  common.  The  variability  of  the 
electrocardiograms  in  aortic  disease  harmonises  with  the 
findings  at  autopsy  ;  these  are  equally  variable.  If  the 
muscle  of  the  separate  ventricles  is  weighed,  an  increase  in  the 
weight  of  the  left  chamber  is  almost  invariably  found,  but  so 
also  is  an  increase  in  the  weight  of  the  right  chamber.  The 
relative  weights  of  the  ventricles,  which  alone  influences  the 


: s 


Fig.   98.     From  a  case  in  which  there  was  conspicuous  displacement  of  the 

heart  towards  the  right  side. 
Fig.   99.     The  curves  of  a  transposed  heart.     All  the  summits  are  inverted 

in  lead  / 


electrocardiogram,  is  normal  in  aortic  disease  almost  as  often 
as  the  normal  ratio  is  disturbed  by  preponderance  of  the  left 
ventricle. 

The  electrocardiograms  which  indicate  deficient  conduc- 
tion through  the  right  division  of  the  bundle  seem  to  be  more 
than  coincidentally  frequent  in  aortic  disease  ;  and  occurring 
in  aortic  disease  they  may  be  misinterpreted.     Fig.  97  serves 


108 


Chapter  X. 


as  an  example.  Now  these  curves  were  taken  at  a  slow  rate, 
and  a  cursory  examination  would  suggest  preponderance  of 
the  left  ventricle.  But  the  initial  phases  of  the  ventricular 
complexes  are  long,  they  together  exceed  a  tenth  of  a  second 
in  duration.  The  direction  of  T1  in  lead  /  and  in  lead  III 
and  the  notching  of  the  downstroke  of  S1  in  lead  II  all  point 
to   a  branch  lesion   (compare   Fig.    18   and    19).     A   second 


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Fig.  100.  From  a  patient  in  whom  there  were  clear  signs  of  congenital 
stenosis  of  the  pulmonary  artery.  Right  ventricular  preponderance  is 
indicated. 


\-"y- 


101.       From   a   patient  who   presented  the   signs   of   a   patent   ductus 
arteriosus.     The  curves  are  normal. 


example  of  the  same  defect  in  aortic  disease  has  been  given 
already  in  Fig.   18. 

Mitral  regurgitation.  The  curves  show  no  constant 
characters. 

Congenital  heart  affections.  These  curves  are  often  of 
value.  The  electrocardiograms,  when  the  heart  is  transposed, 
are  the  most  distinctive  signs  of  the  abnormality  which  we 


Special   Conditions. 


109 


-— 


ijw 


Fig.  102.  From  a  child  in  whom  there  were  signs  of  congenital  pulmonary 
stenosis.  Preponderance  of  the  right  ventricle  is  indicated  in  the  curves. 
Note  the  exaggerated  amplitude  of  excursion  in  leads  /  and  III.  The 
heart  of  this  child  was  subsequently  obtained  ;  pulmonary  stenosis  was 
found  ;  the  left  ventricle  weighed  67  and  the  right  ventricle  161  grammes. 
The  middle  curve  is  from  lead  II  and  not  as  marked. 

Fig.  .103.  From  a  lad  with  a  greatly  enlarged  heart  and  congenital  mal- 
formations. The  chief  signs  were  a  systolic  thrill,  palpable  over  a  wide 
area  and  maximal  at  the  pulmonary  cartilage  ;  a  systolic  murmur, 
prolonged  into  and  enforced  in  diastole,  which  was  maximal  in  the  same 
region  ;  and  a  systolic  apical  murmur.  The  right  carotid  artery  crossed 
the  trachea.     Note  the  increased  excursion  in  leads  II  and  III. 


1 10  Chapter    X. 

possess,  not  excepting  the  skiagram.  All  the  summits  of 
lead  i"  are  inverted  (Fig.  99).  A  little  consideration  will 
make  it  clear  how  this  change  comes  about.  The  lead  is  a 
symmetric  one,  being  from  the  right  arm  to  the  left  arm. 
A  lead  from  the  left  arm  to  the  right  inverts  the  picture  in  the 
normal  subject,  and  the  left  arm  stands  to  the  normal  subject 
as  does  the  right  to  the  subject  of  transposition.  But 
neither  of  the  other  leads  is  symmetric,  and  neither  of  the 
other  leads  shows  inversion.  For  example,  a  lead  from  the 
right  arm  to  the  left  leg  in  any  subject  gives  almost  precisely 
the  same  picture  as  does  a  lead  from  the  right  arm  to  the  right 
lag.  So  it  happens  that  a  lead  from  the  right  arm  to  left  leg 
(lead  //)  in  a  normal  subject  is  almost  equivalent  to  a  lead 
from  the  left  arm  to  the  left  leg  (lead  ///)  in  the  subject  of 
transposition.  In  the  subject  of  transposition,  while  the 
curve  from  lead  I  is  inverted,  those  of  leads  II  and  III  replace 
each  other.  The  value  of  the  transposition  curves  will  be 
evident  ;  displacement  of  the  heart  distorts  electrocardio- 
grams, but  does  not  induce  these  changes.  An  example  of 
extreme  displacement  is  illustrated  by  Fig.  98.  It  was  taken 
from  a  boy  ;  the  heart's  impulse  was  found  well  to  the  right 
of  the  sternum,  and  no  reason  for  displacement  was  apparent. 
The  question  of  transposition  arose,  but  the  electrocardio- 
grams denied  the  presence  of  this  anomaly,  as  did  also  the 
skiagram  ;  the  chief  distortion  is  in  the  opening  ventricular 
events  of  lead  I. 

In  those  children  in  whom  cardiac  enlargement,  cyanosis 
and  harsh  systolic  thrills  and  murmurs,  maximal  over  the 
pulmonary  cartilage,  are  the  chief  diagnostic  signs,  the 
electrocardiograms  generally  indicate  extreme  degrees  of 
right  preponderance.  These  are  instances  of  pulmonary 
stenosis.  Fig.  100  exemplifies  the  curves  of  this  condition  ; 
Fig.  102  is  an  exceptional  example  from  a  similar  case  and 
illustrates  another  feature  of  congenital  heart  curves,  namely, 


Special   Conditions.  Ill 

extreme  amplitude  of  excursion.  Exaggerated  amplitude 
in  several  leads  is  in  itself  a  valuable  sign  of  congenital 
valve  or  septal  defects.  Another  example,  Fig.  103,  shows 
this  increase  of  excursion.  Such  curves  are  obtained, 
so  far  as  I  know,  only  when  there  is  reason  to  believe  that 
congenital  malformation  is  present.  It  is  impossible  to 
speak  at  all  fully  of  these  electrocardiograms  at  the  present 
time  ;  we  require  far  more  information  regarding  them, 
and  especially  a  careful  comparison  with  post-mortem 
material  ;  but  there  are  indications  that  in  the  future  they  will 
he  our  chief  means  of  identifying  anomalies  of  development. 
If  there  is  one  congenital  defect  in  which  the  electric  curves 
should  be  normal,  it  is  in  uncomplicated  patency  of  the  ductus 
-arteriosus.  Fig.  101  was  taken  from  a  youth  who  exhibited 
a  continuous  harsh  murmur  over  the  pulmonary  area.  The 
heart  was  not  enlarged,  and  though  engaged  in  laborious 
work  the  patient  had  experienced  no  symptoms  from  child- 
hood onwards.     The  curves  present  no  abnormality. 

Renal  diseases  and  high  blood  pressure.  The  electro- 
cardiagrams  of  chronic  renal  disease  are  not  distinctive. 
The  curves  may  indicate  preponderance  of  right  or  left 
ventricle,  or  the  relative  amplitudes  of  R  and  S  in  the  several 
leads  may  be  normal.  However,  curves  of  left  preponderance 
are  frequent  in  patients  whose  systolic  blood  pressure  is  high. 
These  records  are  quite  consistent  with  the  ventricular 
weights  in  chronic  renal  disease  ;  these  weights  show  the 
ventricles  to  be  equally  hypertrophied  in  the  average.  Some 
of  the  hearts  show  preponderance  of  the  left  ventricle, 
notably  those  which  have  pumped  against  high  arterial 
pressures  ;  other  hearts  show  right  preponderance.  The 
traditional  teaching  is  that  renal  disease  spells  left 
hypertrophy  ;     but    this    teaching   is    incomplete,    for   right 


112  Chapter    X. 

hypertrophy  of  equal  degree  may  be  shown  by  weighing  the 
separated  ventricles. 

Exophthalmic  goitre.  It  has  been  said  that  T  is 
exaggerated  in  this  condition.  I  have  examined  a  number 
of  patients  and,  apart  from  the  enhanced  rate  of  beat  and 
slight  changes  which  may  result  therefrom,  no  definite 
alterations  have  been  seen  (see  Fig.  56,  78  and  87)  in  the 
shape  of  the  ventricular  complex.  Naturally  irregularities 
of  rhythm  or  changes  in  the  form  of  curve,  consequent  upon 
hypertrophy,  may  be  and  frequently  are  associated  with  this 
disease  from  time  to  time. 


INDEX. 


INDEX. 


Aberrant  contractions 
Aortic  disease  and 

Accelerated  heart  action 

In  exophthalmic  goitre 

In  fever,  with  exercise,  etc. 

Activity  and  negativity 

Age  (Physiological  electrocardiogram  and 

Alternation  of  the  heart 

Alternation  of  the  pulse 

Amplitude  of  deflections 
In  aortic  disease 
In  bundle  branch  lesions 
In  congenital  disease 
In  hypertrophy 
In  mitral  stenosis.  . 

Aortic  disease 

Aberrant  impulses  and 
Hypertrophy  and  .  . 
R  summit  in 
T  summit  in 

Auricular  complex  (see  also  P  summit) 

Auricular  fibrillation 

Complete  heart-block  and.  . 
Digitalis  in 
Heart-block  and 
Irregidarity  in 
Mitral  stenosis  and 
Nature  of   .  . 

Oscillations  of  (see    Oscillations) 
Premature  beats  and 
■  Regular  action  of  the  ventricle  and, 
Transient    .  . 


27,  63,  95 

&  106 

32 

&  106 

66  &  75 

66 

&  112 

66 

15 

22 

98 

98 

21 

106 

27 

111 

30 

103 

106 

30 

&  107 

32 

&  106 

106 

107 

13 

&  17 

85 

93 

93 

93 

86 

105 

85 

86 

95 

93 

91 

116 


Index. 


Auricular  flutter 
Digitalis  in 
Heart-block  and     .  . 
Treatment  of 

AURTCULO- VENTRICULAR    BUNDLE 

Branches  of 

Damage  to  branches  of 

Bigram 

Blood  pressure  raised    .  . 

Bradycardia 


Compensator 

Compensatory  pause 

Complete  heart-block 

Auricular  fibrillation  and 

Compression  op  vagus 

Congenital  heart  affections    .  . 

Constitution  of  ventricular  complex 

Deflection  time 

Dextrogram. . 

Digitalis 

Fibrillation  and 
Flutter  and 
Heart  block  and 
Sino-auricidar  heart-block  and 

Diphasic  effect 

Direction  of  contraction  wave 

"  Dropped  "  beats 


Ectopic  beats 

Ectopic  rhythm 

Electrocardiograms  (see  Physiological  electrocardiograms) 

Escaped  contractions       .  .  .  .  . .  .  .  .  .  . .  .  .  50 

Exercise  (Influence  on  electrocardiograms)         ...         .  .  22  &  66 


75 

82 

76 

82 

18 

&  24 

24 

&  27 

27 

26 

32  &  111 

•• 

47 

7 

54 

43 

93 

79 

108 

24 

11 

26 

93 

82 

43 

98 

16 

16 

37 

52,  54,  60 

68 

&80 

.  .  68, 

74 

&  80 

Index. 


117 


CONTRA!  THINS) 


Exophthalmic  goitre 

Accelerated  heart  action  in 
T  summit  in 
Extras ystoles  (see  Premature 

Flint's  murmur 

Galvanometer  (see  String  galvanometer) 
Galvanometric  circuits  .  . 


Heart-block 

Auricular  fibrillation  and 

Auricular  flutter  and 

Complete 

Partial 

Premature  beats  and 

Sino -auricular 

High  blood  pressure 

Hypertrophy 

Aortic  disease  and 
Mitral  stenosis  and 


Impulses  meeting  in  the  ventricle 

Intermittence 

"  Interpolated  "  beats  . . 


Leads 


Special 
Usual  three 


Levogram 

Limits  of  amplitude 

Mitral  regurgitation 

Mitral  stenosis 

Auricular  fibrillation  and 
Hypertrophy  in 
Oscillations  in 
P  summit  in 
Paroxysmal  tachycardia  and 


66  &   112 
112 


L06 

1 

4 

36 
93 
76 
43 
37 
46 
98 

32  &   111 

30,   103  &   106 
103 


38, 


58 
52  &  98 
58 

5 
89 
6  &  18 

26 

21 


108 

103 
103 
32  &  103 
89  &   103 
: ■■),  61  &  103 
105 


118 


Index. 


Negativity  and  activity 
Newborn  child 
Nodal  rhythm 

Overshooting  of  string 

Oscillations 

In  fibrillation 

Character  of 

Special  leads  to  detect 

Variations  in  amplitude  of 

Oscillations  of  tremor 

P   SUMMIT 

Absence  of  .  . 
Amplitude  of 
Anomalous  forms  of 
Bifurcation  of 
Buried 
Contiguous .  . 
In  mitral  stenosis . 
Meaning  of 

Pacemaker 

Dislocation  of 

Paroxysmal  tachycardia 
Mitral  stenosis  and 
Simple  form  of 
Ventricular  origin  of 

Partial  heart-block 

Clinical  examples  of 

Patent  ductus  arteriosus 

Physiological  electrocardiogram 
Constancy  of 
Influence  of  posture  and  exercise 
Time  relations  of 

Post-paroxysmal  pause 

p-r  interval 

Prolongation  of 
Shortening  of 
Variation  in 


15 

33 

50  &  73 

11 


85 

S7 

89 

87 

89 

13 

50, 

72  &  86 

21 

59, 

68  &  73 

17  &   103 

54  &  71 

.  .    77 

39, 

61  &  103 

17 

36  &  52 

73 

66, 

75  &  91 

105 

66 

..  '   72 

36 

41 

111 

13 

19 

22 

13 

70 

37 

37 

64  &  72 

48  &  73 

38  &  40 

Index. 


119 


Premature  contractions  (Extras ystoles)     . 

52 

Auricular  fibrillation  and 

95 

Auricular  origin 

59 

Heart-block  and 

46  &  64 

.  .Sinus  origin 

61 

Successive 

56,  62  &  68 

Ventricular  origin 

52 

Premature  ventricular  contractions 

52 

Types  of 

56 

Properties  of  the  string 

11 

Pulmonary  stenosis  (congenital) 

32  &  110 

Pulsus  alternans     .  . 

98 

Q    DEPRESSION 

13,  27  &  46 

Amplitude  of 

21 

Nature  of   .  . 

13,  27  &  46 

QBS    GROUP 

18&26 

Bizarre  type  of 

19 

Length  of    .  . 

18&27 

R    SUMMIT 

13  &  27 

Amplitude  in  hypertrophy  of 

32 

Amplitude  of 

21 

Aortic  disease  and 

106 

Bifurcation  of  (notching) 

18 

Increased,  amplitude  of 

32,   106  &   111 

"  Refractory  "  state 

58 

Renal  disease 

Ill 

Respiratory  arrhythmia 

96 

S   DEPRESSION 

13  &  27 

Amplitude  in  hypertrophy  of 

32 

'  '  Amplitude  of 

21 

Bifurcation  (notching)  of .  . 

18 

Increased  amplitude  of     .  . 

32  &   111 

SlNO-AURICULAR    BLOCK 

48  &   98 

Sinus  arrhythmia 

96 

Sinus  Extrasvstoles 

.  .          61 

120 


Index. 


Sinus  irregularities 

96 

Skin  current 

7 

Slow  action  op  the  heart 

..43, 

47  &  9S 

Special  leads 

89 

Standardiser 

7 

Standardised  curves 

..  7  &  9 

Steele's  murmur     .  . 

106 

String  galvanometer 

1 

String  properties 

11 

Superimposed  summits 

40,  45, 

54  &  62 

Supraventricular  impulses 

24,  25,  45,  50, 

59  &  85 

Switchboard 

4 

T  SUMMIT        .  .            . .            .  . 

13 

Amplitude  of 

21 

Aortic  disease  and 

107 

Change  of  shape    . . 

71 

Exophthalmic  goitre  and  . 

112 

Flattened 

105 

Increased  amplitude  of     . 

22  &   112 

Inversion  of 

19 

35  &  95 

Testing  string 

11 

Transposition  of  heart  .  . 

108 

U    SUMMIT        .  .              .  . 

..          19 

Amplitude  of 

21 

Vagal  compression 

79 

Vagal  irregularities 

96 

Valve  lesions 

101 

Ventricular  complex  (see    Q,   j 

%    S   AND     T) 

13  &  27 

In  the  three  leads 

18 

Meaning  of 

17  &  27 

Of  anomalous  forms 

23  &  52 

Physiological 

17 

Variations  in 

18 

SHAW  &i  SONS,  FETTER  LANE,  LONDON,  B.C.4 


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Lewis 

Clinical  electrocardiography. 

fCtrj 


